中点钳位(neutral point clamped,NPC)型三电平逆变器并网工作环境恶劣,IGBT面临单管与双管同时故障的挑战,这使得故障特征之间的差异变得非常微弱,进而导致双管故障的识别精度难以有效提升。为此,提出了一种新的故障诊断方法,该方法结...中点钳位(neutral point clamped,NPC)型三电平逆变器并网工作环境恶劣,IGBT面临单管与双管同时故障的挑战,这使得故障特征之间的差异变得非常微弱,进而导致双管故障的识别精度难以有效提升。为此,提出了一种新的故障诊断方法,该方法结合了多通道的二维递归融合图和轻量化多尺度残差(lightweightmultiscale convolutional residuals,LMCR)网络。首先,通过仿真获取三相电流信号作为故障信号;再利用递归图(recurrence plot,RP)将三相电流信号分别转化为二维图并进行多通道融合,以捕捉时间序列中的周期性、突变点和趋势等特征;最后,将递归融合图作为输入,输入到LMCR模型中进行故障识别,LMCR模型整合多级Inception结构和残差网络,用于提取不同尺度的特征并融合这些特征,从而保证网络的梯度消失和爆炸。实验结果显示,该方法在IGBT故障识别中表现出色,无噪声环境下平均识别准确率达100%,噪声环境中也达到了92.53%,充分证明了该方法具有较强的特征提取能力和优异的抗噪性能。展开更多
Editor's Note:The“two ssions”,the annual ssions of China's national lgislature and political advisory body,kicked of in early March in Beiing.As a highly anticipated event on the country's political cale...Editor's Note:The“two ssions”,the annual ssions of China's national lgislature and political advisory body,kicked of in early March in Beiing.As a highly anticipated event on the country's political calendar,it attracted both domestic and international attentions,ofering a critical window for the world at large into China's achievements in 2024 and is roadmap towards high-quality development and Chinese modernization in 2025-the final year of China's 14th Five Year Plan(2021-2025).展开更多
为降低中点箝位型(neutral point clamped,NPC)三电平整流器的电流谐波,在dq同步旋转坐标系下推导出带中点电压耦合项的NPC三电平整流器数学模型,并分析中点电压对电流控制的影响。对模型中的中点电压耦合项和交流侧等效电阻会增大电流...为降低中点箝位型(neutral point clamped,NPC)三电平整流器的电流谐波,在dq同步旋转坐标系下推导出带中点电压耦合项的NPC三电平整流器数学模型,并分析中点电压对电流控制的影响。对模型中的中点电压耦合项和交流侧等效电阻会增大电流谐波及无法通过常规方法进行准确估计的问题,设计一种混合参数自适应的迭代学习控制方法,以进行解耦控制并消除不确定参数的影响。通过构造Lyapunov函数和理论推导验证控制方法的稳定性。在整流器硬件平台上进行试验验证,结果表明,所设计的控制方法可有效降低电流谐波。展开更多
Objective: The study aimed to explore the protective mechanism of Ganoderic acid A (GAA) in renal fibrosisand to verify that GAA can ameliorate renal fibrosis by regulating the Niemann-pick C1-like 1 (NPC1L1) gene. Meth...Objective: The study aimed to explore the protective mechanism of Ganoderic acid A (GAA) in renal fibrosisand to verify that GAA can ameliorate renal fibrosis by regulating the Niemann-pick C1-like 1 (NPC1L1) gene. Methods:Transforming growth factor beta1 (TGF-β1) was used to treat Human Kidney-2 (HK-2) cells to establish a renal fibrosismodel. The differentially expressed genes in the control (CTRL) group, TGF-β1 group, and TGF-β1 + GAA group werescreened via transcriptome sequencing technology and verified by qPCR and Western blot experiments. The NPC1L1gene overexpression plasmid was constructed. The expression levels of N-cad, E-cad, and Slug-related proteins inCTRL, TGF-β1, TGF-β1+GAA (25 μg/mL), and TGF-β1+GAA (25 μg/mL) + NPC1L1 Overexpression (OE) groupswere detected by qPCR and Western blot analysis. Western blot analysis was used to identify the extracellular matrixassociated proteins Tenascin-C, α-SMA, and fibrosis-related protein Collagen I. Fibrosis marker protein Fibronectinwas detected and quantified by immunofluorescence. Results: Transcriptomic sequencing revealed that TGF-β1stimulation led to 267 differentially regulated genes, with 118 up-regulated and 149 down-regulated, while furthermodulation of 213 genes, comprising 112 up-regulated and 101 down-regulated genes, was observed in the GAAintervention group. The target gene in these processes was found to be NPC1L1 by investigations using GeneOntology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). qPCR and Western blot resultsconfirmed that TGF-β1 increased NPC1L1 expression, which was attenuated by GAA. Additionally, TGF-β1upregulated N-cad and Slug. However, GAA reversed this effect and NPC1L1 overexpression partially rescued theGAA effect. TGF-β1 also decreased E-cad expression, reversed by GAA, and NPC1L1 overexpression antagonized thisreversal. Furthermore, TGF-β1 promoted Collagen I, α-SMA, and Tenascin-C expression, and GAA reduced theselevels, effects that were reversed by NPC1L1 overexpression. Immunofluorescence results showed that TGF-β1increased fibronectin expression, which was decreased by GAA, and increased by NPC1L1 overexpression.Conclusion: GAA ameliorates renal fibrosis by antagonizing NPC1L1 gene expression inhibiting epithelialmesenchymal transition and reducing extracellular matrix formation.展开更多
Intervertebral disc degeneration(IVDD),a disease associated with ageing,is characterised by a notable increase in senescent nucleus pulposus cells(NPCs)as IVDD progresses.However,the specific mechanisms that regulate ...Intervertebral disc degeneration(IVDD),a disease associated with ageing,is characterised by a notable increase in senescent nucleus pulposus cells(NPCs)as IVDD progresses.However,the specific mechanisms that regulate the senescence of NPCs remain unknown.In this study,we observed impaired autophagy in IVDD-NPCs,which contributed to the upregulation of NPCs senescence and the senescence-associated secretory phenotype(SASP).The dysregulated SASP disrupted NPCs viability and initiated extracellular matrix degradation.Conversely,the restoration of autophagy reversed the senescence phenotype by inhibiting GATA binding protein 4(GATA4).Moreover,we made the novel observation that a cross-talk between histone H3 lysine 4 trimethylation(H3K4me3)modification and N6-methyladenosine(m6A)-methylated modification regulates autophagy in IVDD-NPCs.Mechanistically,lysine methyltransferase 2A(KMT2A)promoted the expression of methyltransferase-like 3(METTL3)through H3K4me3 modification,whereas METTL3-mediated m6A modification reduced the expression of autophagy-associated 4a(ATG4a)by attenuating its RNA stability,leading to autophagy damage in NPCs.Silencing KMT2A and METTL3 enhanced autophagic flux and suppressed SASP expression in IVDD-NPCs.Therefore,targeting the H3K4me3-regulated METTL3/ATG4a/GATA4 axis may represent a promising new therapeutic strategy for IVDD.展开更多
文摘Editor's Note:The“two ssions”,the annual ssions of China's national lgislature and political advisory body,kicked of in early March in Beiing.As a highly anticipated event on the country's political calendar,it attracted both domestic and international attentions,ofering a critical window for the world at large into China's achievements in 2024 and is roadmap towards high-quality development and Chinese modernization in 2025-the final year of China's 14th Five Year Plan(2021-2025).
文摘为降低中点箝位型(neutral point clamped,NPC)三电平整流器的电流谐波,在dq同步旋转坐标系下推导出带中点电压耦合项的NPC三电平整流器数学模型,并分析中点电压对电流控制的影响。对模型中的中点电压耦合项和交流侧等效电阻会增大电流谐波及无法通过常规方法进行准确估计的问题,设计一种混合参数自适应的迭代学习控制方法,以进行解耦控制并消除不确定参数的影响。通过构造Lyapunov函数和理论推导验证控制方法的稳定性。在整流器硬件平台上进行试验验证,结果表明,所设计的控制方法可有效降低电流谐波。
基金sponsored by KeyResearch and Development Project of Science andTechnology Department of Tibet (No. XZ202201ZY0033G).
文摘Objective: The study aimed to explore the protective mechanism of Ganoderic acid A (GAA) in renal fibrosisand to verify that GAA can ameliorate renal fibrosis by regulating the Niemann-pick C1-like 1 (NPC1L1) gene. Methods:Transforming growth factor beta1 (TGF-β1) was used to treat Human Kidney-2 (HK-2) cells to establish a renal fibrosismodel. The differentially expressed genes in the control (CTRL) group, TGF-β1 group, and TGF-β1 + GAA group werescreened via transcriptome sequencing technology and verified by qPCR and Western blot experiments. The NPC1L1gene overexpression plasmid was constructed. The expression levels of N-cad, E-cad, and Slug-related proteins inCTRL, TGF-β1, TGF-β1+GAA (25 μg/mL), and TGF-β1+GAA (25 μg/mL) + NPC1L1 Overexpression (OE) groupswere detected by qPCR and Western blot analysis. Western blot analysis was used to identify the extracellular matrixassociated proteins Tenascin-C, α-SMA, and fibrosis-related protein Collagen I. Fibrosis marker protein Fibronectinwas detected and quantified by immunofluorescence. Results: Transcriptomic sequencing revealed that TGF-β1stimulation led to 267 differentially regulated genes, with 118 up-regulated and 149 down-regulated, while furthermodulation of 213 genes, comprising 112 up-regulated and 101 down-regulated genes, was observed in the GAAintervention group. The target gene in these processes was found to be NPC1L1 by investigations using GeneOntology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). qPCR and Western blot resultsconfirmed that TGF-β1 increased NPC1L1 expression, which was attenuated by GAA. Additionally, TGF-β1upregulated N-cad and Slug. However, GAA reversed this effect and NPC1L1 overexpression partially rescued theGAA effect. TGF-β1 also decreased E-cad expression, reversed by GAA, and NPC1L1 overexpression antagonized thisreversal. Furthermore, TGF-β1 promoted Collagen I, α-SMA, and Tenascin-C expression, and GAA reduced theselevels, effects that were reversed by NPC1L1 overexpression. Immunofluorescence results showed that TGF-β1increased fibronectin expression, which was decreased by GAA, and increased by NPC1L1 overexpression.Conclusion: GAA ameliorates renal fibrosis by antagonizing NPC1L1 gene expression inhibiting epithelialmesenchymal transition and reducing extracellular matrix formation.
基金supported by the National Natural Science Foundation of China (82272555,82272522,82422044,82101647)Zhejiang Provincial Natural Science Foundation of China (LGF21H060010,LR22H060001,LY23H060011)+1 种基金Wenzhou Major Scientific and Technological Innovation Project (ZY2022010)Zhejiang Provincial Medical Technology Foundation of China (2022PY071)。
文摘Intervertebral disc degeneration(IVDD),a disease associated with ageing,is characterised by a notable increase in senescent nucleus pulposus cells(NPCs)as IVDD progresses.However,the specific mechanisms that regulate the senescence of NPCs remain unknown.In this study,we observed impaired autophagy in IVDD-NPCs,which contributed to the upregulation of NPCs senescence and the senescence-associated secretory phenotype(SASP).The dysregulated SASP disrupted NPCs viability and initiated extracellular matrix degradation.Conversely,the restoration of autophagy reversed the senescence phenotype by inhibiting GATA binding protein 4(GATA4).Moreover,we made the novel observation that a cross-talk between histone H3 lysine 4 trimethylation(H3K4me3)modification and N6-methyladenosine(m6A)-methylated modification regulates autophagy in IVDD-NPCs.Mechanistically,lysine methyltransferase 2A(KMT2A)promoted the expression of methyltransferase-like 3(METTL3)through H3K4me3 modification,whereas METTL3-mediated m6A modification reduced the expression of autophagy-associated 4a(ATG4a)by attenuating its RNA stability,leading to autophagy damage in NPCs.Silencing KMT2A and METTL3 enhanced autophagic flux and suppressed SASP expression in IVDD-NPCs.Therefore,targeting the H3K4me3-regulated METTL3/ATG4a/GATA4 axis may represent a promising new therapeutic strategy for IVDD.
