为研究车用质子交换膜燃料电池的预测和健康管理问题,提出了一种以相对功率损耗率为健康指标、灰狼优化(grey wolf optimizer,GWO)算法与径向基(radial basis function,RBF)神经网络相结合的方法(GWO-RBF),对车用质子交换膜燃料电池的...为研究车用质子交换膜燃料电池的预测和健康管理问题,提出了一种以相对功率损耗率为健康指标、灰狼优化(grey wolf optimizer,GWO)算法与径向基(radial basis function,RBF)神经网络相结合的方法(GWO-RBF),对车用质子交换膜燃料电池的剩余使用寿命进行预测。首先,通过对初始时刻燃料电池极化曲线的分析,构建以相对功率损耗率为健康指标的计算方法,并采用灰色关联度分析方法验证其可行性。然后,应用GWO算法优化的RBF神经网络预测车用质子交换膜燃料电池的剩余使用寿命。最后,采用两组数据集对提出的方法进行了验证分析。结果表明:与其他方法相比,提出的基于GWO-RBF方法的平均绝对百分比误差、均方根误差最小,决定系数最大,相对误差小于1%。可见本文方法能够以较少的数据集、较高的精度预测车用质子交换膜燃料电池的剩余使用寿命。展开更多
OBJECTIVE Lychee seed,a famous traditional Chinese medicine,recently were reported to improve the learning and memory abilities in mice.However,it is still unclear whether lychee seed saponins(LSS)can improve the cogn...OBJECTIVE Lychee seed,a famous traditional Chinese medicine,recently were reported to improve the learning and memory abilities in mice.However,it is still unclear whether lychee seed saponins(LSS)can improve the cognitive function and associated mechanisms.METHODS In present studies,we established the Alzheimer disease(AD)model by injecting Aβ25-35 into the lateral ventricle of rats.Then the spatial learning and memory abilities of LSS-treated rats were evaluated with the Morris water maze,meanwhile the protein expressions of AKT,GSK3β and Tau in the hippocampal neuron were analyzed by immunohistochemistry and Western blotting.RESULTS The results showed LSS can improve the cognitive functions of AD rats through shortening the escape latency,increasing the number across the platform,platform quadrant dwell time and the percentage of the total distance run platform quadrant.The protein expression of AKT was significantly up-regulated and that of GSK3β and Tau were decreased remarkably in the hippocampal CA1 area.CONCLUSION Our study is the first to show that LSS significantly improve the cognitive function and prevent hippocampal neuronal injury of the rats with AD by activation of the PI3K/AKT/GSK3βsignaling pathway,suggesting LSS may be developed into the nutrient supplement for the treatment of AD.展开更多
Background Dendritic cells(DCs)are the most important antigen-presenting cells due to their professional and extremely efficient antigen-presenting function.The dynamics of cytoskeleton plays crucial regulated roles o...Background Dendritic cells(DCs)are the most important antigen-presenting cells due to their professional and extremely efficient antigen-presenting function.The dynamics of cytoskeleton plays crucial regulated roles on DCs’immune functions and biophysical properties.Several evidences show that tumor-derived suppressive cytokines deteriorate DCs’immune functions through remodeling their F-actin cytoskeleton.But the underlying mechanism is still elusive.Tropomodulin1(Tmod1),a cytoskeleton-binding protein,regulates and stabilizes actin filaments lengths and cytoskeleton architecture,which involves in the regulations of the morphology,formation of neural dendrites and biophysical properties of cells.Our previous studies found that mature DCs(mDCs)had a higher expression of Tmod1 than immature DCs(imDCs). Therefore,it’s hypothesized that Tmod1 maybe involve in the modification of DCs’functions.Objective The aim of the study is to investigate the effects of Tmodl on the immune functions and biophysical properties of DCs and the underlying mechanisms in order to further understand the biological behaviors of DCs.Methods Bone marrow-derived cells were harvested from wild type(C57BL/6 J)mice and Tmod1 knockout mice(Tmod1 overexpressing transgenic(TOT)/Tmod1-/-)and differentiated to immature dendritic cells(imDCs)by rmGM-CSF and rmIL-4.imDCs were then matured by lipopolysaccharides(LPS)treatment.The expressions of the surface markers in DCs,including CD80,CD86,CD40,MHC-Ⅱand CCR7,were detected by flow cytometry,Western blot and qRT-PCR.The inflammation cytokines such as IL-6,IFN-γ,IFN-βand IL-10 were also detected by flow cytometry.The immune functions and the biophysical properties of DCs were compared between the wild type and Tmod1 knockout mice.The F-actin content and dendritic pseudopodia of these two kinds of DCs were detected by flow cytometry and laser scanning confocal microscope respectively.Finally,we detected the MyD88 dependent and independent signaling pathway to discover the molecular mechanisms.Results We found that Tmod1-deficient mDCs showed deficient antigen-presenting ability and they failed to express enough MHC-Ⅱ,co-stimulated molecules(CD80/86,CD40)and CCR7 on their cell surface.The secretions of the inflammatory cytokines IL-6 and IFN-γwere decreased while the anti-inflammatory cytokines IFN-βand IL-10 were increased in the supernatant of Tmod1-deficient mDCs.As compared to DCs of wild type mice,the migration ability of DCs from Tmod1 knockout mice were dramatically damaged including their free migration and CCL19 mediated chemotaxis migration.However,we found that Tmod1 knockout had no effects on the imDCs’endocytosis ability.Furthermore,Tmod1 knockout DCs showed higher osmotic fragility,lower Young’s modulus,less F-actin content and shorter dendritic pseudopodia.Under LPS stimulation,the phosphorylation level of p65 and p38 were significantly downregulated in Tmod1 knockout mice while the expression of p-IRF3 was upregulated.Conclusions These results indicated that Tmodl knockout leads to deficient antigen-presenting ability and impaired migration of DCs as well as their biophysical properties.The underlying mechanisms are due to the inhibitions of the TLR4-mediated NF-κB and p38 MAPK singling pathway and the activation of the IRF3 signaling pathway,as well as the disturbed reorganization of the F-actin cytoskeleton.Our results provide a new insight on the functions of Tmod1 which can affect the DCs’immune functions and biophysical properties through regulating the TLR4-mediated singling pathways and cytoskeleton remodeling.展开更多
A practical method of estimation for the internal-resistance of polymer electrolyte membrane fuel cell (PEMFC) stack was adopted based on radial basis function (RBF) neural networks. In the training process, k-means c...A practical method of estimation for the internal-resistance of polymer electrolyte membrane fuel cell (PEMFC) stack was adopted based on radial basis function (RBF) neural networks. In the training process, k-means clustering algorithm was applied to select the network centers of the input training data. Furthermore, an equivalent electrical-circuit model with this internal-resistance was developed for investigation on the stack. Finally using the neural networks model of the equivalent resistance in the PEMFC stack, the simulation results of the estimation of equivalent internal-resistance of PEMFC were presented. The results show that this electrical PEMFC model is effective and is suitable for the study of control scheme, fault detection and the engineering analysis of electrical circuits.展开更多
Direct carbon solid oxide fuel cells(DC-SOFCs)are promising,green,and efficient power-generating devices that are fueled by solid carbons and comprise all-solid-state structures.Developing suitable anode materials for...Direct carbon solid oxide fuel cells(DC-SOFCs)are promising,green,and efficient power-generating devices that are fueled by solid carbons and comprise all-solid-state structures.Developing suitable anode materials for DC-SOFCs is a substantial scientific challenge.Herein we investigated the use of La_(0.75)Sr_(0.25)Cr_(0.5)Mn_(0.5)O_(3)-δ−Ce_(0.8)Gd_(0.2)O_(1.9)(LSCM−GDC)composite electrodes as anodes for La_(0.9)Sr_(0.1)Ga_(0.8)Mg_(0.2)O_(3)-δelectrolyte-based DC-SOFCs,with Camellia oleifera shell char as the carbon fuel.The LSCM−GDC-anode DC-SOFC delivered a maximum power density of 221 mW/cm^(2) at 800℃ and it significantly improved to 425 mW/cm^(2) after Ni nanoparticles were introduced into the LSCM−GDC anode through wet impregnation.The microstructures of the prepared anodes were characterized,and the stability of the anode in a DC-SOFC and the influence of catalytic activity on open circuit voltage were studied.The above results indicate that LSCM–GDC anode is promising to be applied in DC-SOFCs.展开更多
OBJECTIVE MicroR NA(miR NA)holds promise as a novel therapeutic tool for cancer treatment.However,the transfection efficiency of current delivery systems represents a bottleneck for clinical applications.Here,we demon...OBJECTIVE MicroR NA(miR NA)holds promise as a novel therapeutic tool for cancer treatment.However,the transfection efficiency of current delivery systems represents a bottleneck for clinical applications.Here,we demonstrate that gap junctions mediate an augmentative effect on the antiproliferation mediated by mi R-124-3p in U87 and C6 glioblastoma cells.METHODS The functional inhibition of gap junctions using either si RNA or pharmacological inhibition eliminated the mi R-124-3p-mediated antiproliferation,whereas the enhancement of gap junctions with retinoic acid treatment augmented this mi R-124-3p-mediated antiproliferation.A similar effect was observed in glioblastoma xenograft models.RESULTS More importantly,patch clamp and co-culture assays demonstrated the transmission of mi R-124-3p through gap junction channels into adjacent cells.In further exploring the impact of gap junction-mediated transport of mi R-124-3p on mi R-124-3p target pathways,we found that mi R-124-3p inhibited glioblastoma cell growth in part by decreasing the protein expression of cyclindependent kinase 6,leading to cel cycle arrest at the G0/G1phase;moreover,pharmacological regulation of gap junctions affected this cell cycle arrest.CONCLUSION Our results indicate that the″bystander″effects of functional gap junctions composed of connexin 43 enhance the antitumor effect of mi R-124-3p in glioblastoma cells by transferring mi R-124-3p to adjacent cells,thereby enhancing G0/G1cell cycle arrest.These observations provide a new guiding strategy for the clinical application of mi RNA therapy in tumor treatment.展开更多
文摘为研究车用质子交换膜燃料电池的预测和健康管理问题,提出了一种以相对功率损耗率为健康指标、灰狼优化(grey wolf optimizer,GWO)算法与径向基(radial basis function,RBF)神经网络相结合的方法(GWO-RBF),对车用质子交换膜燃料电池的剩余使用寿命进行预测。首先,通过对初始时刻燃料电池极化曲线的分析,构建以相对功率损耗率为健康指标的计算方法,并采用灰色关联度分析方法验证其可行性。然后,应用GWO算法优化的RBF神经网络预测车用质子交换膜燃料电池的剩余使用寿命。最后,采用两组数据集对提出的方法进行了验证分析。结果表明:与其他方法相比,提出的基于GWO-RBF方法的平均绝对百分比误差、均方根误差最小,决定系数最大,相对误差小于1%。可见本文方法能够以较少的数据集、较高的精度预测车用质子交换膜燃料电池的剩余使用寿命。
基金supported by Science and Technology Planning Project of Sichuan Province(2008SZ0050,14JC0798)Educational Commission of Sichuan Province(10ZA035,15ZA0155)+1 种基金Science and Technology Program of Luzhou(2015-S-43,2016LZXNYD-T03)Key Development Program of Southwest Medical University(2010ZD-010)
文摘OBJECTIVE Lychee seed,a famous traditional Chinese medicine,recently were reported to improve the learning and memory abilities in mice.However,it is still unclear whether lychee seed saponins(LSS)can improve the cognitive function and associated mechanisms.METHODS In present studies,we established the Alzheimer disease(AD)model by injecting Aβ25-35 into the lateral ventricle of rats.Then the spatial learning and memory abilities of LSS-treated rats were evaluated with the Morris water maze,meanwhile the protein expressions of AKT,GSK3β and Tau in the hippocampal neuron were analyzed by immunohistochemistry and Western blotting.RESULTS The results showed LSS can improve the cognitive functions of AD rats through shortening the escape latency,increasing the number across the platform,platform quadrant dwell time and the percentage of the total distance run platform quadrant.The protein expression of AKT was significantly up-regulated and that of GSK3β and Tau were decreased remarkably in the hippocampal CA1 area.CONCLUSION Our study is the first to show that LSS significantly improve the cognitive function and prevent hippocampal neuronal injury of the rats with AD by activation of the PI3K/AKT/GSK3βsignaling pathway,suggesting LSS may be developed into the nutrient supplement for the treatment of AD.
基金funded by the National Natural Science Foundation of China ( 31660258,31771014, 31860262,31570938,31260227)the Science and Technology Foundation of Guizhou Province ( 2019-2787,2018-1412, 2016-5676,2017-5718)+2 种基金the Science and Technology Innovative Talent Team of Guizhou Province ( 2015-4021)the 2011 Collaborative Innovation Program of Guizhou Province ( 2015-04 )the Cell and Gene Engineering Innovative Research Groups of Guizhou Province ( KY-2016-031)
文摘Background Dendritic cells(DCs)are the most important antigen-presenting cells due to their professional and extremely efficient antigen-presenting function.The dynamics of cytoskeleton plays crucial regulated roles on DCs’immune functions and biophysical properties.Several evidences show that tumor-derived suppressive cytokines deteriorate DCs’immune functions through remodeling their F-actin cytoskeleton.But the underlying mechanism is still elusive.Tropomodulin1(Tmod1),a cytoskeleton-binding protein,regulates and stabilizes actin filaments lengths and cytoskeleton architecture,which involves in the regulations of the morphology,formation of neural dendrites and biophysical properties of cells.Our previous studies found that mature DCs(mDCs)had a higher expression of Tmod1 than immature DCs(imDCs). Therefore,it’s hypothesized that Tmod1 maybe involve in the modification of DCs’functions.Objective The aim of the study is to investigate the effects of Tmodl on the immune functions and biophysical properties of DCs and the underlying mechanisms in order to further understand the biological behaviors of DCs.Methods Bone marrow-derived cells were harvested from wild type(C57BL/6 J)mice and Tmod1 knockout mice(Tmod1 overexpressing transgenic(TOT)/Tmod1-/-)and differentiated to immature dendritic cells(imDCs)by rmGM-CSF and rmIL-4.imDCs were then matured by lipopolysaccharides(LPS)treatment.The expressions of the surface markers in DCs,including CD80,CD86,CD40,MHC-Ⅱand CCR7,were detected by flow cytometry,Western blot and qRT-PCR.The inflammation cytokines such as IL-6,IFN-γ,IFN-βand IL-10 were also detected by flow cytometry.The immune functions and the biophysical properties of DCs were compared between the wild type and Tmod1 knockout mice.The F-actin content and dendritic pseudopodia of these two kinds of DCs were detected by flow cytometry and laser scanning confocal microscope respectively.Finally,we detected the MyD88 dependent and independent signaling pathway to discover the molecular mechanisms.Results We found that Tmod1-deficient mDCs showed deficient antigen-presenting ability and they failed to express enough MHC-Ⅱ,co-stimulated molecules(CD80/86,CD40)and CCR7 on their cell surface.The secretions of the inflammatory cytokines IL-6 and IFN-γwere decreased while the anti-inflammatory cytokines IFN-βand IL-10 were increased in the supernatant of Tmod1-deficient mDCs.As compared to DCs of wild type mice,the migration ability of DCs from Tmod1 knockout mice were dramatically damaged including their free migration and CCL19 mediated chemotaxis migration.However,we found that Tmod1 knockout had no effects on the imDCs’endocytosis ability.Furthermore,Tmod1 knockout DCs showed higher osmotic fragility,lower Young’s modulus,less F-actin content and shorter dendritic pseudopodia.Under LPS stimulation,the phosphorylation level of p65 and p38 were significantly downregulated in Tmod1 knockout mice while the expression of p-IRF3 was upregulated.Conclusions These results indicated that Tmodl knockout leads to deficient antigen-presenting ability and impaired migration of DCs as well as their biophysical properties.The underlying mechanisms are due to the inhibitions of the TLR4-mediated NF-κB and p38 MAPK singling pathway and the activation of the IRF3 signaling pathway,as well as the disturbed reorganization of the F-actin cytoskeleton.Our results provide a new insight on the functions of Tmod1 which can affect the DCs’immune functions and biophysical properties through regulating the TLR4-mediated singling pathways and cytoskeleton remodeling.
基金Project (2003AA517020) supported by the National High-Tech Research and Development Program of China
文摘A practical method of estimation for the internal-resistance of polymer electrolyte membrane fuel cell (PEMFC) stack was adopted based on radial basis function (RBF) neural networks. In the training process, k-means clustering algorithm was applied to select the network centers of the input training data. Furthermore, an equivalent electrical-circuit model with this internal-resistance was developed for investigation on the stack. Finally using the neural networks model of the equivalent resistance in the PEMFC stack, the simulation results of the estimation of equivalent internal-resistance of PEMFC were presented. The results show that this electrical PEMFC model is effective and is suitable for the study of control scheme, fault detection and the engineering analysis of electrical circuits.
基金Project(2019YFC1907405)supported by the National Key R&D Program of ChinaProject(GJJ200809)supported by the Education Department Project Fund of Jiangxi Province,ChinaProject(2020BAB214021)supported by the Natural Science Foundation of Jiangxi Province,China。
文摘Direct carbon solid oxide fuel cells(DC-SOFCs)are promising,green,and efficient power-generating devices that are fueled by solid carbons and comprise all-solid-state structures.Developing suitable anode materials for DC-SOFCs is a substantial scientific challenge.Herein we investigated the use of La_(0.75)Sr_(0.25)Cr_(0.5)Mn_(0.5)O_(3)-δ−Ce_(0.8)Gd_(0.2)O_(1.9)(LSCM−GDC)composite electrodes as anodes for La_(0.9)Sr_(0.1)Ga_(0.8)Mg_(0.2)O_(3)-δelectrolyte-based DC-SOFCs,with Camellia oleifera shell char as the carbon fuel.The LSCM−GDC-anode DC-SOFC delivered a maximum power density of 221 mW/cm^(2) at 800℃ and it significantly improved to 425 mW/cm^(2) after Ni nanoparticles were introduced into the LSCM−GDC anode through wet impregnation.The microstructures of the prepared anodes were characterized,and the stability of the anode in a DC-SOFC and the influence of catalytic activity on open circuit voltage were studied.The above results indicate that LSCM–GDC anode is promising to be applied in DC-SOFCs.
基金The project supported by National Natural Science Foundation of China(81473234,U1303221)
文摘OBJECTIVE MicroR NA(miR NA)holds promise as a novel therapeutic tool for cancer treatment.However,the transfection efficiency of current delivery systems represents a bottleneck for clinical applications.Here,we demonstrate that gap junctions mediate an augmentative effect on the antiproliferation mediated by mi R-124-3p in U87 and C6 glioblastoma cells.METHODS The functional inhibition of gap junctions using either si RNA or pharmacological inhibition eliminated the mi R-124-3p-mediated antiproliferation,whereas the enhancement of gap junctions with retinoic acid treatment augmented this mi R-124-3p-mediated antiproliferation.A similar effect was observed in glioblastoma xenograft models.RESULTS More importantly,patch clamp and co-culture assays demonstrated the transmission of mi R-124-3p through gap junction channels into adjacent cells.In further exploring the impact of gap junction-mediated transport of mi R-124-3p on mi R-124-3p target pathways,we found that mi R-124-3p inhibited glioblastoma cell growth in part by decreasing the protein expression of cyclindependent kinase 6,leading to cel cycle arrest at the G0/G1phase;moreover,pharmacological regulation of gap junctions affected this cell cycle arrest.CONCLUSION Our results indicate that the″bystander″effects of functional gap junctions composed of connexin 43 enhance the antitumor effect of mi R-124-3p in glioblastoma cells by transferring mi R-124-3p to adjacent cells,thereby enhancing G0/G1cell cycle arrest.These observations provide a new guiding strategy for the clinical application of mi RNA therapy in tumor treatment.
