Research on Fault Current Controller of DC Microgrid

[Introduction] With the rapid development of AC/DC distribution networks and distributed generation technology, the role of DC microgrids in distribution networks is becoming increasingly important and will become an important component of future distribution networks. Due to the small coverage area and low line impedance of the DC microgrid, when an inter pole short circuit fault occurs, the fault current increases rapidly and has a large amplitude, which can reach more than 10 times the rated working current. This makes it difficult to set the protection of DC microgrids and requires high equipment selection, which restricts the rapid development of DC microgrids. [Method] In response to the above issues, taking the DC microgrid as the research object, starting from the working principle of inter pole faults in the DC microgrid, the fault characteristics on the DC side of the DC microgrid were analyzed. In response to the shortcomings of existing main current limiting methods, a voltage controllable fault current controller was proposed to achieve precise control of fault current. The simulation model of DC microgrid and fault current controller was built for simulation verification. [Result] The simulation results show that the fault current controller can significantly reduce the fault current and achieve precise control of the fault current, making the system controllable before and after the fault without locking the protection. During steady-state operation, the fault current controller can also assist the VSC (Voltage Source Converter) in further stabilizing the DC bus voltage. [Conclusion] To cooperate with the normal operation of the relay protection device and avoid VSC triggering overcurrent protection blocking, it is recommended to set the fault current control range between 1~2 pu

Lysophosphatidic Acid Is Associated with Atherosclerotic Plaque Instability by Regulating NF-κB Dependent Matrix Metalloproteinase-9 Expression via LPA2 in Macrophages

Lysophosphatidic acid (LPA), one of the simplest phospholipid signaling molecules, participates in formation and disruption of atherosclerotic plaque. Matrix metalloproteinases (MMPs) contribute to atherosclerotic plaque rupture by involving in extracellular matrix (ECM) degradation and then thinning fibrous cap. Our previous study demonstrated that macrophage-derived MMP-9 was associated with coronary plaque instability, but the relationship between LPA and MMP-9 remains unclear. The present work therefore aimed at elucidating association between LPA and MMP-9 and the regulation mechanism of LPA on MMP-9 in macrophages. We found that plasma LPA and MMP-9 levels were correlated positively (r = 0.31, P < 0.05) and both elevated significantly in patients with acute myocardial infarct (AMI). Consistent with peripheral blood levels, histochemical staining indicated that autotaxin (ATX), LPA-producing ectoenzyme, and MMP-9 were expressed frequently in the necrotic core and fibrous cap of human unstable plaques, which might increase the instability of plaque. Experiments in vitro were done with THP-1-derived macrophages and showed that LPA enhanced the expression, secretion and activity of MMP-9 in a time- and dose-dependent manner. Induction of LPA on pro-MMP-9 and active-MMP-9 was confirmed in human peripheral blood monocyte-derived macrophages. PDTC, NF-κB inhibitor, but not inhibitor of AP-1 and PPARγ, effectively prevented LPA-induced MMP-9 expression and NF-κB p65 siRNA decreased MMP-9 transcription, confirming that LPA might induce MMP-9 elevation by activating NF-κB pathway. In addition, knockdown of LPA2 attenuated LPA-induced MMP-9 expression and nucleus p65 levels. These findings revealed that LPA upregulated the expression of MMP-9 through activating NF-κB pathway in the LPA2 dependent manner, hence blocking LPA receptors signaling may provide therapeutic strategy to target plaque destabilization

Growth inhibition of mesenchymal stem cells by aspirin: involvement of the wnt/

SUMMARY 1. Mesenchymal stem cell (MSC) therapy is drawing increasing attention in cardiology. However, the effect of aspirin, an assistant medication used extensively in the treatment of cardiovascular diseases, on MSC is not clear. 2. In the present study, we investigated the effect of aspirin on the growth of MSC in vitro and the underlying mechanism of its action

Hydrogen Sulfide Promotes Cardiomyocyte Proliferation and Heart Regeneration via ROS Scavenging

Neonatal mouse hearts can regenerate completely in 21 days after cardiac injury, providing an ideal model to exploring heart regenerative therapeutic targets. The oxidative damage by Reactive Oxygen Species (ROS) is one of the critical reasons for the cell cycle arrest of cardiomyocytes (CMs), which cause mouse hearts losing the capacity to regenerate in 7 days or shorter after birth. As an antioxidant, hydrogen sulfide (H2S) plays a protective role in a variety of diseases by scavenging ROS produced during the pathological processes. In this study, we found that blocking H2S synthesis by PAG (H2S synthase inhibitor) suspended heart regeneration and CM proliferation with ROS deposition increase after cardiac injury (myocardial infarction or apex resection) in 2-day-old mice. NaHS (a H2S donor) administration improved heart regeneration with CM proliferation and ROS elimination after myocardial infarction in 7-day-old mice. NaHS protected primary neonatal mouse CMs from H2O2-induced apoptosis and promoted CM proliferation via SOD2-dependent ROS scavenging. The oxidative DNA damage in CMs was reduced with the elimination of ROS by H2S. Our results demonstrated for the first time that H2S promotes heart regeneration and identified NaHS as a potent modulator for cardiac repair

Sex-related differences in the association between plasma fibrinogen and non-calcified or mixed coronary atherosclerotic plaques

Abstract Background Plasma fibrinogen (FIB) has been demonstrated to be a risk factor for cardiovascular disease. Patients with non-calcified plaque (NCP) or mix plaque (MP) have a higher risk of poor outcomes. However, the association between FIB and the presence of NCP or MP (NCP/MP) remains unclear, and if present, whether sex has any impact on this association remains unknown. The aim of this study was to investigate the role of FIB in predicting the presence of NCP/MP and evaluate whether sex has any impact on this association. Methods A total of 329 subjects were recruited, and the clinical and laboratory data were collected. Plasma FIB was detected by enzyme-linked immunosorbent assay. According to whether they had coronary atherosclerotic plaques and the characteristics of the most stenotic plaque, we divided them into three groups: no plaque (NP), calcified plaque (CP), and NCP/MP. Results Patients with NCP/MP had significantly higher FIB level in females, but not in males. Multiple logistic regression analysis showed that FIB was an independent risk factor for the presence of NCP/MP (odds ratio [OR] = 3.677, 95% CI 1.539–8.785, P = 0.003) in females. Receiver operating characteristic (ROC) curve analysis showed that the optimal cut-off value FIB for predicting the presence of NCP/MP was 3.41 g/L (area under curve [AUC] = 0.73, 95% CI 0.63–0.82, P <  0.001) in females. Conclusions FIB is independently associated with the presence of NCP/MP in females, but not in males. These results suggest that the potential significance of FIB-lowering regimens in females with NCP/MP

Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol

Background: We previously reported that lysophosphatidic acid (LPA) promoted cardiomyocyte hypertrophy in vitro via one of its G protein-coupled receptor subtypes, LPA3. In this study, we examined the role of LPA3 in cardiac hypertrophy induced by isoproterenol (ISO) and myocardial infarction.Methods:In vitro, neonatal rat cardiomyocytes (NRCMs) were subjected to LPA3 knocked-down, or pretreated with a β-adrenergic receptor (β-AR) antagonist (propranolol) before LPA/ISO treatment. Cardiomyocyte size and hypertrophic gene (ANP, BNP) mRNA levels were determined. In vivo, LPA3-/- and wild-type mice were implanted subcutaneously with an osmotic mini-pump containing ISO or vehicle for 2 weeks; echocardiography was performed to determine the heart weight/body weight ratio, cardiomyocyte cross-sectional area, and level of ANP mRNA expression. LPA3-/- and wild-type mice were subjected to permanent coronary artery ligation or sham surgery for 4 weeks; cardiac function, including the degree of hypertrophy and infarction size, was determined.Results:In vitro, we found that knocked-down LPA3 in NRCMs did not attenuate ISO-induced hypertrophy, and propranolol was unable to abolish LPA-induced hypertrophy. In vivo, chronic ISO infusion caused cardiac hypertrophy in wild-type mice, while hypertrophic responses to ISO infusion were not attenuated in LPA3-/- mice. However, in a myocardial infarction (MI) model, LPA3-/- mice exhibited reduced cardiac hypertrophy compared to wild-type mice at 4 weeks post-MI, which was associated with reduced cardiac function and increased infarct size.Conclusions: Our data show that LPA3 appears to play a protective role in myocardial hypertrophy post-MI, but does not appear to be involved in the hypertrophy that occurs in response to β-AR stimulation in vivo and in vitro. These results implicate LPA-LPA3 lipid signaling in cardiac hypertrophy occurring after pathological insults like MI, which presents a new variable in β-AR-independent hypertrophy. Thus, modulation of LPA3 signaling might represent a new strategy for preventing the stressed myocardium from ischemia injury

Genome-wide identification and expression analysis of the ZIP gene family in Quercus dentata

The ZIP (Zn-regulated, iron-regulated transporter-like protein) gene family is a novel metal transporter that is capable of absorbing and transporting a variety of metal cations, including zinc (Zn), iron (Fe), manganese (Mn), and cadmium (Cd). Quercus dentata Thunb. is a candidate plant species for the phytoremediation of heavy metal contaminated soil. A chromosome-scale genome assembly is reported recently for Q. dentata, however, genome-wide analysis of ZIP genes has not been performed. In this study, we identified 29 ZIP genes in Q. dentata genome using bioinformatics tools. The sequence homology, chromosomal distribution and phylogenetic relationship of these genes with ZIP genes from other plants indicated potential gene duplication during Q. dentata genome evolution. Sequence analysis revealed 23 conserved motifs in QdZIP proteins and 11 types of high-frequency cis-acting elements in the promoters of QdZIP genes. QdZIP proteins were predicted to localize on cell membrane except QdZIP7. QdZIP7 was predicted to be a chloroplast protein, which was confirmed using microscopic observation of QdZIP7-GFP fusion protein. QdZIP gene expression patterns in roots and exophytic mycorrhiza, leaves, stems and fruits were obtained from transcriptome data, and the responsiveness of QdZIP7 to excessive heavy metal Zn was detected using qRT-PCR. In summary, our study provided a basic sights on the ZIP gene family in Q. dentata, laying the foundation for in-depth investigation on the roles of the ZIP proteins in heavy metal transport