Biological rhythms play a critical role in regulating human physiology and have been implicated in the onset, progression, and recovery of ischemic stroke (IS). This review summarizes recent experimental and clinical studies that associate circadian regulation with post-stroke blood-brain barrier (BBB) repair, focusing on the role of molecular clock components. Core clock components, including BMAL1 and CLOCK, influence BBB integrity by regulating tight junction protein expression, angiogenesis, neuroimmune responses, and neuroendocrine signaling. Finally, we discuss emerging chronotherapeutic strategies that integrate circadian biology into stroke rehabilitation.

BACKGROUND:Hypertensive intracerebral hemorrhage (HICH) is a critical neurological emergency associated with high morbidity and mortality. Conventional Western medical therapies - such as antihypertensive treatment, intracranial pressure reduction, and supportive care - provide symptomatic relief but remain limited in promoting hematoma absorption, neurological recovery, and long-term functional outcomes. Traditional Chinese medicine (TCM) has shown clinical potential in enhancing neurological repair and improving prognosis. Given their complementary strengths, combined Chinese and Western medicine may represent a more comprehensive treatment strategy. However, the overall efficacy and safety of such integrative approaches remain uncertain due to inconsistent findings and lack of high-quality evidence. METHODS:A comprehensive search of CNKI, VIP, CBM, PubMed Embase, and Cochrane Library was conducted from 2010 to March 2024. Randomized controlled trials (RCTs) comparing combined therapy with Western medicine alone were included. The primary outcome was overall clinical effective rate. Secondary outcomes included National Institutes of Health Stroke Scale (NIHSS) score, Glasgow Coma Scale (GCS) score, hs-CRP level, adverse events and mortality. Data extraction, risk-of-bias assessment using the Cochrane tool and statistical analyses were independently performed by 2 reviewers. Meta-analysis was conducted with fixed- or random-effects models depending on heterogeneity, while sensitivity, subgroup, publication bias and trial sequential analyses (TSA) were also performed. RESULTS:Eighteen RCTs involving 1644 participants were analyzed. Compared with Western medicine alone, combined therapy significantly improved clinical effective rate (OR = 4.35, 95% CI [3.08-6.13], P < .00001), NIHSS score (MD = -2.95, 95% CI [-2.29 to -1.95], P < .00001), GCS score (MD = 1.95, 95% CI [1.61-2.28], P < .00001), and reduced hs-CRP levels (MD = -1.31, 95% CI [-1.44 to -1.19], P < .00001). No significant difference was observed in adverse events (OR = 0.81, P = .43). Mortality was reported in only one trial and showed no difference between groups (P > .05). TSA supported the sufficiency and robustness of evidence for the primary outcome. CONCLUSION:The therapeutic effect of combined traditional Chinese and Western medicine in treating HICH is better than that of Western medicine alone.

BACKGROUND:Stroke is a leading cause of death and disability worldwide, yet its treatment still faces significant challenges. Mendelian randomization (MR) has been widely used to discover new biomarkers and therapeutic targets. This study aimed to identify therapeutic targets for stroke within the plasma proteome range using MR. METHODS:We conducted a two-sample MR study, evaluating the causal relationships between 2,940 plasma proteins from the UK Biobank-Proteome-wide Association Study (UKB-PPP) and stroke, with further validation in 4,907 plasma proteins from Iceland. Subsequently, drug target proteins were determined using Bayesian colocalization, Summary data-based Mendelian randomization (SMR), and protein-protein interaction (PPI) network construction to validate the role of selected disease-associated proteins. RESULTS:Preliminary MR analysis identified 11 proteins (LPA, FURIN, MST1, FKBPL, SH2B3, MMP12, F11, ITGAV, DDHD2, VSIR and GAS6) significantly associated with stroke or stroke subtypes. Through SMR and colocalization analysis, 4 potential drug target proteins were identified: FURIN as a potential drug target for stroke and any ischemic stroke, F11 as a potential drug target for cardioembolic stroke, DDHD2 and VSIR as potential drug targets for small vessel stroke. It is worth noting that F11 is currently being used in the development of multiple drugs, FURIN is not only associated with stroke but also appears to have abnormal expression in several cardiovascular diseases. Although research on DDHD2 and VSIR in the context of stroke is relatively limited, current findings indicate that DDHD2 is related to synaptic plasticity, while VSIR is associated with microglia and immune responses. CONCLUSION:This study found that the plasma proteins FURIN, F11, DDHD2, and VSIR show promise as potential therapeutic targets for stroke and its subtypes, providing genetic evidence to support precision drug development and insights into the underlying pathological mechanisms of stroke. CLINICAL TRIAL NUMBER:Not applicable.

Ischemic stroke ranks as the second leading cause of global mortality and disability. Although reperfusion is crucial for salvaging brain tissue, it carries the risk of secondary injuries, such as ferroptosis. Gastrodin, a neuroprotective compound found in Chinese herbal medicine, may regulate this process. However, its impact on stroke-induced ferroptosis remains unclear. OBJECTIVE:This research endeavors to probe Gastrodin's influence on post-ischemic ferroptosis, deciphering its mechanisms and assessing its therapeutic promise. METHODS:We developed rat models of middle cerebral artery occlusion/reperfusion (MCAO/R) and created oxygen-glucose deprivation/reoxygenation (OGD/R)-damaged PC12 cell models. Gastrodin was administered to assess ferroptosis using Prussian blue staining and fluorescence probes. To investigate the effects of gastrodin on the xCT/GPX4 and ACSL4/LPCAT3 pathways, we employed molecular docking, immunofluorescence, Western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, we used transmission electron microscopy and JC-1 fluorescence probes to examine mitochondrial integrity and function. RESULTS:Our study demonstrated that gastrodin significantly reduced iron accumulation and lipid peroxidation in the brains of MCAO/R rats and OGD/R-injured PC12 cells. It suppressed reactive oxygen species (ROS) and ameliorated mitochondrial membrane potential. It potentiates the xCT/GPX4 axis while repressing the ACSL4/LPCAT3 pathway, leading to improved mitochondrial architecture and function, notably characterized by decreased mitochondrial membrane potential, reduced ROS levels, and increased formation of mitochondrial cristae. By modulating the xCT/GPX4 and ACSL4/LPCAT3 pathways, gastrodin mitigated ferroptosis in ischemic stroke, thereby preserving mitochondrial structural and functional integrity. This study provides novel mechanistic insights into gastrodin's therapeutic potential for treating ischemic stroke, highlighting the importance of traditional Chinese medicine in modern medical therapy.

ETHNOPHARMACOLOGICAL SIGNIFICANCE:Huoxue Rongluo Formula (HXRLF) is a traditional Chinese medicine prescription widely used to treat ischemic stroke (IS), based on the classical therapeutic principles of nourishing yin and activating blood circulation. Preliminary clinical studies have demonstrated its effectiveness in improving neurological function and prognosis. However, the precise mechanisms by which HXRLF confers neuroprotection, especially its role in modulating ferroptosis after cerebral ischemia-reperfusion injury (CIRI), remain unclear. AIM OF THE STUDY:This study aimed to investigate whether HXRLF ameliorates cerebral I/R injury by inhibiting neuronal ferroptosis through NR4A1-mediated activation of the xCT/GPX4 antioxidant axis. MATERIALS AND METHODS:Active components of HXRLF were identified by UPLC-Q-TOF-MS. UPLC-Q-TOF-MS analysis revealed several representative active constituents of HXRLF, including catalpol, chebulic acid, didymin, armepavine, harpagoside, atractylenolide III, poncirin, and coclaurine, which together represent the diverse chemical basis underlying its pharmacological actions. Potential anti-ferroptosis targets were screened using network pharmacology and GEO transcriptomic data. A transient middle cerebral artery occlusion (tMCAO) model in mice and an OGD/R model in HT22 cells were used to evaluate the neuroprotective effects of HXRLF. Biochemical assays, immunofluorescence, transmission electron microscopy (TEM), and Western blotting were employed to detect ferroptosis-related indicators. The role of NR4A1 was further examined using its antagonist DIM-C-pPhOH, and the downstream involvement of ferroptosis was confirmed by the ferroptosis inhibitor Fer-1. RESULTS:HXRLF significantly improved neurobehavioral outcomes, reduced infarct volume, and alleviated pathological damage in tMCAO mice in a dose-dependent manner. Biochemical assays revealed that HXRLF reduced Fe2+ and MDA levels while increasing GSH content in brain tissue. HXRLF treatment also restored GPX4 expression and mitochondrial structure. In HT22 cells, HXRLF-containing serum improved cell viability, reversed lipid peroxidation, reduced iron accumulation, and restored mitochondrial membrane potential. Mechanistically, HXRLF upregulated NR4A1 and enhanced the expression of xCT and GPX4. Importantly, the neuroprotective and anti-ferroptotic effects of HXRLF were diminished by NR4A1 inhibition and partially rescued by Fer-1, confirming the involvement of the NR4A1-xCT-GPX4 axis in ferroptosis regulation. CONCLUSION:HXRLF ameliorates cerebral I/R injury by inhibiting neuronal ferroptosis through NR4A1-mediated activation of the xCT/GPX4 antioxidant axis. These findings provide mechanistic insights into the neuroprotective effects of traditional Chinese medicine and offer a scientific foundation for developing ferroptosis-targeted therapies in ischemic stroke.

ETHNOPHARMACOLOGICAL RELEVANCE:Ischemic stroke (IS) a complex pathological event emerging as one of the most serious threats with huge economic impact in the 21st century. Following IS, multiple cascades and pathways are stimulated, culminating in long term consequences. One of Chinese Traditional Medicine, Tianma Siwu Decoction (TSD), is known to have sedative-hypnotic, anticonvulsant and anti-inflammatory effects, which is usually used to treat migraine and ischemic stroke, but its potential pharmacological mechanism remains unclear. AIM OF THE STUDY:This study is aimed to identify the active principles from TSD that has strong pharmacological effect on the treatment of IS. MATERIALS AND METHODS:Based on liquid chromatography-triple quadrupole mass spectrometry (LC-Q-MS/MS) technology, a new three-step-based approach integrating concentration parameters and Quality marker (Q-marker) with network pharmacology and bioactivity evaluation to explore the therapeutic effects and mechanisms of TSD on ischemic stroke. Ultimately, as the main herb of the TSD, high-concentration compounds from Gastrodia elata Blume (GEB) were identified and collected by LC-Q-MS/MS, and an optimized analytical model in multidimensional network pharmacology was introduced to more accurately explore the potential mechanisms by which TSD affects IS. RESULTS:The results showed that 280 overlapping targets of TSD were obtained after the introduction of compound concentration parameters into the multidimensional network pharmacology analysis. Additionally, TSD might regulate IS through the AGE-RAGE and Rap1 signaling pathways. Through an in vitro hypoxia-reoxygenation injury cell model, it was discovered that as the Q-markers of GEB, gastrodin and parishin could effectively reduce neuronal hypoxic injury by modulating the expression levels of p-JNK and p-p38 proteins. According to the results of molecular docking, gastrodin and baicalin exhibits strong binding affinity to GAPDH and MAPK3, respectively (≦-7 kcal/mol). CONCLUSION:We discovered that compound concentration is a key factor that influence the activity of substances, affects the accuracy and reliability of predictive outcomes. Consequently, the study enhances the network pharmacology model by incorporating concentration factors, aiming for a more accurate understanding of the potential mechanisms behind TSD anti-ischemic stroke actions.

Background: Ischemic stroke leads to significant neuronal damage, and impaired angiogenesis remains a critical factor limiting post-stroke recovery. Ginkgolide B (GB), a key component of Ginkgo biloba extract, has shown potential neuroprotective effects, but its pro-angiogenic mechanisms remain unclear. Methods: To investigate the effects of GB, we established an oxygen–glucose deprivation/reperfusion (OGD/R) model using bEnd.3 cells. Potential molecular targets of GB were explored through a combination of network pharmacology analysis, protein–protein interaction (PPI) network construction, pathway enrichment, and molecular dynamics simulations. Based on these predictions, a series of in vitro assays—including Cell Counting Kit-8 (CCK-8), 5-ethynyl-2′-deoxyuridine (EdU) incorporation, wound-healing, Transwell migration, and Matrigel tube formation tests—were performed to evaluate cell viability, proliferation, migration, and angiogenic activity. Western blotting was conducted to detect AKT serine/threonine kinase 1 (AKT1), vascular endothelial growth factor (VEGF), and Angiogenin (Ang) expression and clarify the role of the AKT1/VEGF/Ang pathway. Results: Bioinformatics analysis identified 19 potential targets, among which AKT1, Matrix Metalloproteinase 9 (MMP9), and Prostaglandin-Endoperoxide Synthase 2 (PTGS2) exhibited the highest relevance. GB showed no evident cytotoxicity at concentrations up to 40 μM and mitigated the OGD/R-induced reduction in cell viability. At this concentration range, GB also enhanced endothelial proliferation, migration, and tube formation in bEnd.3 cells. Mechanistic studies revealed that MK2206 inhibition of AKT1 markedly suppressed AKT1 expression (p < 0.01), impaired angiogenic capacity, and aggravated ischemic–hypoxic injury, whereas GB treatment significantly increased VEGF and Ang expression (p < 0.01), likely via AKT1 upregulation (p < 0.01). Conclusion: GB promotes angiogenesis and exerts neuroprotective effects by activating the AKT1/VEGF/Ang signaling pathway, suggesting its potential therapeutic value for ischemic stroke–related injuries.

ETHNOPHARMACOLOGICAL SIGNIFICANCE:Hydroxysafflor yellow A (HSYA), an active constituent extracted from the traditional Chinese herb safflower (Carthamus tinctorius L.), has been used in stroke therapy for centuries and is well known for its anti-inflammatory and neuroprotective properties. However, the mechanisms through which HSYA mitigates Secondary Brain Injury (SBI) following intracerebral hemorrhage (ICH) remain incompletely understood. AIM OF THE STUDY:This study provides a systematic evaluation of the neuroprotective effects of HSYA against SBI, with a particular focus on elucidating its regulatory role in the necroptosis pathway. MATERIALS AND METHODS:An ICH model was established in Sprague-Dawley (SD) rats via autologous blood injection. The neuroprotective efficacy of HSYA was evaluated using the modified neurological severity score (mNSS), monitoring of body weight, and measurement of brain water content to assess cerebral edema, complemented by histological and molecular analyses (TUNEL, ELISA, immunofluorescence (IF), and Western blot). Molecular dynamics simulation (MD) and molecular docking were performed to characterize the binding properties of HSYA with key necroptosis-related proteins, including phospho-receptor-interacting protein kinase 1(p-RIPK1), phospho-receptor-interacting protein kinase 3(p-RIPK3), and phospho-mixed lineage kinase-like protein(p-MLKL). An in vitro ICH model was generated using hemin-stimulated BV2 cells. The effects of HSYA were examined by assessing cell viability, quantifying inflammatory cytokines (TNF-α, IL-1β, IL-6), and determining the expression of necroptosis-associated proteins and inflammatory mediators (TNF-α, high mobility group box-1(HMGB1)). RESULTS:In vivo, HSYA treatment markedly improved mNSS scores and alleviated neuroinflammation, microglial activation, as well as both apoptotic and necroptotic cell death. MD and molecular docking analyses further demonstrated that HSYA exhibits stable binding to the critical phosphorylation sites of receptor-interacting protein kinase 1(RIPK1), receptor-interacting protein kinase 3(RIPK3), and mixed lineage kinase-like protein (MLKL), primarily through interactions involving its hydroxyl groups and aromatic ring structures. Consistently, in vitro experiments showed that HSYA enhanced BV2 cell viability, reduced the release of pro-inflammatory cytokines, and attenuated both apoptosis and necroptosis in hemin-stimulated BV2 cell. CONCLUSION:HSYA may alleviate neurological dysfunction associated with SBI following ICH, potentially by suppressing microglial activation and modulating the necroptosis pathway, thereby interrupting the "inflammation-necroptosis-secondary inflammation" cascade. These findings provide preliminary experimental evidence supporting HSYA as a promising neuroprotective candidate for the treatment of SBI.

This study assesses causal relationships between serum trace elements/nutrients and insomnia using Mendelian randomization (MR) methods. Data was collected from genome-wide association studies, single-nucleotide polymorphisms associated with serum trace elements (iron, zinc, selenium, copper, calcium, potassium, magnesium) and nutrients (carotene, folate, vitamin A, vitamin B12, vitamin B6, vitamin C, vitamin D, vitamin E) were selected as instrumental variables for a 2-sample MR analysis, using insomnia genome-wide association study summary statistics from FinnGen. The primary analysis employed the inverse variance weighted method, supplemented by MR-Egger regression (MR-Egger), weighted median (WME), simple mode, and weighted mode approaches. Causal effects were estimated using inverse variance weighted-derived P-values, odds ratios (ORs), and 95% confidence intervals (CIs). Sensitivity analyses evaluated pleiotropy (MR-Egger intercept test), heterogeneity (Cochran Q test), and robustness (leave-one-out analysis). The OR and 95% CI indicated a possible causal link between magnesium levels and insomnia risk (OR = 0.869, 95% CI = 0.763-0.990, P < .05). No significant causal associations were observed for other serum trace elements or nutrients. Horizontal pleiotropy was assessed using MR-Egger and Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO), with no evidence of bias (MR-Egger intercept P > .05; MR-PRESSO global test P > .05). Cochran Q test revealed no heterogeneity, and leave-one-out analysis confirmed the stability of the causal effect. These sensitivity analyses collectively support the robustness of the Mendelian randomization results. MR analysis indicated a potential association between magnesium concentration and insomnia risk. However, further research is needed to elucidate the underlying biological mechanisms and establish the clinical significance of these associations.

A network traffic prediction system based on the modified LSTM algorithm was devised in response to the constraints of the standard BFS algorithm in space-ground integrated information network traffic prediction. Initial steps in developing a network traffic prediction scheme include precisely localizing influencing components using gating mechanism theory, properly dividing indicators to decrease interference, and finally, building the scheme using the upgraded LSTM algorithm. The experimental findings demonstrate that the suggested scheme outperforms the conventional BFS algorithm under certain assessment criteria, particularly with regard to the processing time of influencing variables and the accuracy of network traffic predictions. The ability to effectively forecast and optimize the development characteristics and product creation of the space-ground integrated information network is enabled by network traffic prediction, which plays a crucial role in this network. When it comes to tackling traffic simulation challenges, the classic BFS method has its limits, particularly when dealing with complicated situations. To address this issue more effectively, this research proposes a network traffic prediction technique that is based on an upgraded LSTM algorithm. This technique makes use of the upgraded LSTM algorithm to build itself after precisely locating the influencing components using the gating mechanism theory in order to decide the division of indicators. Under certain assessment conditions, the experimental findings reveal that the scheme's speed and accuracy are much enhanced for various tasks, and it performs better overall. Hence, for the purpose of improving the simulation accuracy and efficiency in space-ground integrated information network traffic prediction, a method based on the upgraded LSTM algorithm is preferable to the classic BFS algorithm.

Neuroinflammatory responses play an important role in the pathogenesis of various diseases, particularly those affecting the central nervous system. Inhibition of neuroinflammation is a crucial therapeutic strategy for the management of central nervous system disorders. The intestinal microbial-gut-brain axis serves as a key regulatory pathway that modulates neuroinflammatory processes. Intestinal flora metabolites such as short-chain fatty acids, indoles and their derivatives, lipopolysaccharides, trimethylamine oxide, and secondary bile acids exert direct or indirect effects on neuroinflammation. Studies have shown that electroacupuncture (EA) modulates the composition of the intestinal microbiota and its metabolites, while also suppressing neuroinflammation by targeting the TLR4/NF- κ B, NLRP3/caspase-1, and microglial cell M2-type transformation pathways. This review discusses the mechanisms by which EA regulates neuroinflammation via intestinal microbiota and its metabolites, providing information and a foundation for further investigation of the precise therapeutic mechanisms of EA in neurological disorders.

Background: Ischemic stroke (IS) is a major cause of death and disability worldwide. Previous studies have reported associations between metabolic disorders and IS. However, evidence regarding the causal relationship between blood metabolites and IS lacking.Methods: A two-sample Mendelian randomization analysis (MR) was used to assess the causal relationship between 1,400 serum metabolites and IS. The inverse variance-weighted (IVW) method was employed to estimate the causal effect between exposure and outcome. Additionally, MR-Egger regression, weighted median, simple mode, and weighted mode approaches were employed as supplementary comprehensive evaluations of the causal effects between blood metabolites and IS. Tests for pleiotropy and heterogeneity were conducted.Results: After rigorous selection, 23 known and 5 unknown metabolites were identified to be associated with IS. Among the 23 known metabolites, 13 showed significant causal effects with IS based on 2 MR methods, including 5-acetylamino-6-formylamino-3-methyluracil, 1-ribosyl-imidazoleacetate, Behenoylcarnitine (C22), N-acetyltyrosine, and N-acetylputrescine to (N (1) + N (8))-acetate,these five metabolites were positively associated with increased IS risk. Xanthurenate, Glycosyl-N-tricosanoyl-sphingadienine, Orotate, Bilirubin (E,E), Bilirubin degradation product, C17H18N2O, Bilirubin (Z,Z) to androsterone glucuronide, Bilirubin (Z,Z) to etiocholanolone glucuronide, Biliverdin, and Uridine to pseudouridine ratio were associated with decreased IS risk.Conclusion: Among 1,400 blood metabolites, this study identified 23 known metabolites that are significantly associated with IS risk, with 13 being more prominent. The integration of genomics and metabolomics provides important insights for the screening and prevention of IS.

Background:Annao Pingchong decoction (ANPCD) is a traditional Chinese decoction which has definite effects on treating intracerebral hemorrhage (ICH) validated through clinical and experimental studies. However, the impact of ANPCD on oxidative stress (OS) after ICH remains unclear and is worth further investigating.Aim:To investigate whether the therapeutic effects of ANPCD on ICH are related to alleviating OS damage and seek potential targets for its antioxidant effects.Materials and Methods:The therapeutic candidate genes of ANPCD on ICH were identified through a comparison of the target genes of ANPCD, target genes of ICH and differentially expressed genes (DEGs). Protein-protein interaction (PPI) network analysis and functional enrichment analysis were combined with targets-related literature to select suitable antioxidant targets. The affinity between ANPCD and the selected target was verified using macromolecular docking. Subsequently, the effects of ANPCD on OS and the selected target were further investigated through in vivo experiments.Results:Forty-eight candidate genes were screened, in which silent information regulator sirtuin 1 (SIRT1) is one of the core genes that has antioxidant effects and ICH significantly affected its expression. The good affinity between 6 compounds of ANPCD and SIRT1 was also demonstrated by macromolecular docking. The results of in vivo experiments demonstrated that ANPCD significantly decreased modified neurological severity scoring (mNSS) scores and serum MDA and 8-OHdG content in ICH rats, while significantly increasing serum SOD and CAT activity, complicated with the up-regulation of ANPCD on SIRT1, FOXO1, PGC-1α and Nrf2. Furthermore, ANPCD significantly decreased the apoptosis rate and the expression of apoptosis-related proteins (P53, cytochrome c and caspase-3).Conclusion:ANPCD alleviates OS damage and apoptosis after ICH in rats. As a potential therapeutic target, SIRT1 can be effectively regulated by ANPCD, as are its downstream proteins.

Abstract Regarding the sustained issues of commutation failures in the hybrid double-fed DC system encompassing Line Commutated Converter High Voltage Direct Current (LCC-HVDC) and Modular Multilevel Converter High Voltage Direct Current (MMC-HVDC, from the perspective of harmonics, the harmonics in the voltage waveform of the AC bus on the inverter side are analyzed. Besides, a commutation failure suppression strategy for the hybrid doubly-fed DC transmission system based on the minimum shutdown area is designed, in which the setting value of the shutdown angle of the harmonic is considered in the minimum shutdown area. The reactive power is obtained by attaching the setting value to the reactive power control link of MMC-HVDC, and the simulation analysis in PSCAD verifies that the strategy can make the MMC-HVDC output more reactive power during the fault in the weak AC system. Increasing the shut-off margin of the manifold reduces the potential for continuous commutation failures in LCC-HVDC.

A large number of power electron devices involved in the new energy grid-connected system are easy to cause problems such as broadband oscillation, which brings certain risks to the safe operation of the power grid. At present, on the issue of broadband oscillation suppression, the parameter setting schemes of direct-drive permanent magnet wind turbine (D-PMSG) machine / grid side controller (GSC / MSC) and flexible direct current transmission (VSC-HVDC) send / receive controller (SEC / REC) need to be further studied. This paper first analyzes the oscillation mode caused by the new energy access system based on the characteristic root method, and then designs the additional damping controller and uses its parameters as the optimization variable, and uses the coupled oscillation mode as the improvement goal to construct the overall optimization model of the controller parameters. After that, the improved simulated plant algorithm (I-PGSA) based on cloud model theory is used to solve the optimal additional controller parameters. At the same time, in order to prevent the target from shifting during the optimization process, mode tracking technology is introduced to ensure the rationality of the optimization. Finally, the optimization effect of the control parameters is compared through eigenvalue analysis, and the effectiveness of the proposed strategy is verified based on PSCAD / EMTDC emulation.

A common-mode (CM)-conducted electromagnetic interference (EMI) noise, exhibiting characteristics similar to a pulse signal, is produced during the rapid rise and fall of the drain-to-source voltage of the switching device. In order to eliminate the above CM-conducted EMI, a reverse pulse signal, which is denoted by a synchronous pulsed compensation (SPC) signal, is proposed in this article. First, high-frequency equivalent circuits, based on a SiC half-bridge module, are built to determine the time-domain CM-conducted EMI noise. Then, the impact of digital filter circuits with/without SPC signals on CM EMI noise is analyzed through the calculation of insertion loss (IL). In addition, the design of the SPC signal is described in detail. To implement SPC, a digital active EMI filter (DAEF) system is constructed. Next, the overall experimental setup is elaborated upon. The measurements, performed on a 1000-W buck dc-dc converter prototype, finally confirm the SPC method for CM-conducted EMI suppression in the lower-to-medium frequency range.

With the wide application of large-scale photovoltaic power generation system, subsynchronous oscillation below the synchronous frequency has become an important problem affecting the stability of the power system and the safety of equipment. In order to reduce the risk of subsynchronous oscillation in photovoltaic grid-connected systems, this paper proposes a method to suppress subsynchronous oscillation in photovoltaic grid-connected systems by additional damping control of photovoltaic inverters. The additional damping control is introduced into the control link of the PV inverter with the DC voltage as the feedback input signal, so as to enhance the sub-synchronous mode damping of the PV grid-connected system. In addition, the suppression effect of different access positions of the damping controller is analyzed and compared, and the access position with the best suppression effect is proposed.

Ischemic stroke is a major public health problem worldwide. Although the circadian clock is involved in the process of ischemic stroke, the exact mechanism of the circadian clock in regulating angiogenesis after cerebral infarction remains unclear. In the present study, we determined that environmental circadian disruption (ECD) increased the stroke severity and impaired angiogenesis in the rat middle cerebral artery occlusion model, by measuring the infarct volume, neurological tests, and angiogenesis-related protein. We further report that Bmal1 plays an irreplaceable role in angiogenesis. Overexpression of Bmal1 promoted tube-forming, migration, and wound healing, and upregulated the vascular endothelial growth factor (VEGF) and Notch pathway protein levels. This promoting effect was reversed by the Notch pathway inhibitor DAPT, according to the results of angiogenesis capacity and VEGF pathway protein level. In conclusion, our study reveals the intervention of ECD in angiogenesis in ischemic stroke and further identifies the exact mechanism by which Bmal1 regulates angiogenesis through the VEGF-Notch1 pathway.

目的 比较川芎清脑颗粒治疗慢性脑缺血伴头痛的疗效.方法 选择2017年1月1日至2019年12月31日哈尔滨医科大学附属第二医院等5家医院诊治的慢性脑缺血伴头痛患者224例作为研究对象.采用随机数字分组法将患者分成对照组和试验组(各112例).两组患者均接受基础治疗,包括控制血压和对症等治疗,均给予阿司匹林口服100 mg,1次/d.对照组患者使用吡拉西坦治疗,口服0.8 mg,1次/d,连续治疗2个月.试验组患者口服川芎清脑颗粒治疗,10 g/次,3次/d,连续治疗2个月.在治疗前后比较两组患者疼痛情况、认知功能、头痛频次、临床疗效.结果 治疗前两组患者VAS评分差异比较无统计学意义(P＞0.05).在治疗1个月和2个月后试验组患者VAS评分(2.51±0.12,1.87±0.17)均低于对照组(P＜0.05).治疗前两组患者MoCA评分差异比较无统计学意义(P＞0.05).在治疗1个月和2个月后试验组患者MoCA评分(24.69±4.65,28.65±4.15)均高于对照组(P＜0.05).在治疗1个月和2个月后试验组患者头痛频次(1.69±0.41,0.68±0.12)低于对照组(P＜0.05).试验组临床总有效率明显高于对照组(P＜0.05).结论 川芎清脑颗粒治疗慢性脑缺血伴头痛可以明显提升临床疗效,改善患者头痛症状、减少头痛次数、保护患者认知功能.

Ethnopharmacological relevance: Intracerebral hemorrhage (ICH) is a central nervous system disease that causes severe disability or death. Even though Annao Pingchong decoction (ANPCD), a traditional Chinese decoction, has been used clinically to treat ICH in China, its molecular mechanism remains unclear. Aim of the study: To study whether the neuroprotective effect of ANPCD on ICH rats is achieved by alleviating neuroinflammation. This paper mainly explored whether inflammation-related signaling pathways (HMGB1/ TLR4/NF-kappa B P65) plays a role in ANPCD treatment of ICH rats.Materials and methods: Liquid chromatography-tandem mass spectrometry was used to analyze the chemical composition of ANPCD. ICH models were established by injecting autologous whole blood into the left caudate nucleus of Sprague-Dawley (SD) rats. Modified neurological severity scoring (mNSS) was used to assess the neurological deficits. The levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and IL-6 were analyzed using enzyme-linked immunosorbent assay (ELISA). Pathological changes in the rat brains were observed using hematoxylin-eosin, Nissl, and TUNEL staining. The protein levels of HMGB1, TLR4, NF-kappa B p65, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) were measured by western blotting and immunofluorescence analysis.Results: Ninety-three ANPCD compounds were identified, including 48 active plasma components. Treatment with ANPCD effectively improved the outcome, as observed by the neurological function scores analysis and brain histopathology. Our results showed that ANPCD exerts its anti-inflammatory effects by significantly downregulating the expression of HMGB1, TLR4, NF-kappa B p65, TNF-alpha, IL-1 beta, and IL-6. ANPCD also exerted anti-apoptotic effects by significantly decreasing the apoptosis rate and Bax/Bcl-2 ratio. Conclusion: We found that ANPCD had neuroprotective effect in clinical work. Here, we also found that the action mechanism of ANPCD might be related to attenuate neuroinflammation and apoptosis. These effects were achieved by inhibiting the expression of HMGB1, TLR4 and NF-kappa B p65.