The mitochondrial Permeability Transition Pore (mPTP) has been implicated in cell death, energy failure, and oxidative stress. Emerging evidence suggests that mPTP may also contribute to the development and maintenance of chronic pain, although evidence remains limited and the underlying mechanisms are not fully understood. This narrative review summarizes current findings from experimental and clinical chronic pain models and discusses how mPTP-mediated mitochondrial dysfunction may promote central sensitization and pain persistence through reactive oxygen species accumulation, neuroinflammation, apoptosis, and metabolic failure. Pharmacological strategies targeting mPTP and their therapeutic implications are further discussed. Finally, future perspectives are proposed, including mechanistic investigations, drug discovery, and clinical translation. This review highlights mPTP as a promising therapeutic target and provides a focused framework for future studies exploring mitochondrial mechanisms in chronic pain.

Aiming at the difficulties in establishing mechanism models, significant influence of load disturbances on control accuracy, and high requirements for operational smoothness of propulsion systems for chemical tankers under complex sea conditions and liquid cargo sloshing conditions, a Model-Free Adaptive Predictive Control (MFAPC) method incorporating variable-gain error feedback correction is proposed. First, the mathematical model of the chemical tanker’s propulsion motor and propeller load is established. Then, based on the compact-form dynamic linearization technique, the pseudo partial derivative is identified online using system I/O data streams, reconstructing the nonlinear data-driven model and multi-step ahead prediction equations of the propulsion system. A performance index function incorporating rotational speed tracking error and control increment constraints is constructed, and the model-free adaptive predictive control law is designed through rolling optimization. Finally, to address potential control deviations caused by persistent load disturbances, a variable-gain error feedback correction term is introduced into the controller, which adjusts the feedback intensity in real time according to the rotational speed error. Simulation results demonstrate that the proposed control method effectively improves the dynamic response speed and steady-state accuracy of the chemical tanker’s propulsion system, achieves smooth rotational speed regulation, and exhibits excellent control performance.

To address the frequency fluctuation problem in green inland port microgrids caused by the high penetration of distributed energy resources and the frequent switching of large-impact loads such as quay cranes and gantry cranes, a virtual synchronous generator (VSG)–based secondary frequency control strategy employing model-free adaptive predictive control is proposed. The rotor motion equation of the VSG is discretized, and a compact-form dynamic linearization approach is adopted to establish a discrete data-driven model between the VSG output angular frequency and the virtual mechanical power. On this basis, a model-free adaptive predictive controller is designed, in which the system dynamic characteristics are adaptively characterized through online updating of pseudo partial derivatives, and the optimal adjustment of the virtual mechanical power is obtained within the prediction horizon, thereby improving both the dynamic frequency response and steady-state regulation performance. Simulation studies conducted in the MATLAB/Simulink environment verify the effectiveness and stability of the proposed method under impact loads and complex operating conditions.

The complex nature of pain pathophysiology complicates the establishment of objective diagnostic criteria and targeted treatments. The heterogeneous manifestations of pain stemming from various primary diseases contribute to the complexity and diversity of underlying mechanisms, leading to challenges in treatment efficacy and undesirable side effects. Recent evidence suggests the presence of apoptotic cells at injury sites, the distal dorsal root ganglia (DRG), spinal cord, and certain brain regions, indicating a potential link between the ineffective clearance of dead cells and debris and pain persistence. This review highlights recent research findings indicating that efferocytosis plays a significant yet often overlooked role in lesion expansion while also representing a potentially reversible impairment that could be targeted therapeutically to mitigate chronic pain progression. We examine recent advances into how efferocytosis, a process by which phagocytes clear apoptotic cells without triggering inflammation, influences pain initiation and intensity in both human diseases and animal models. This review summarizes that efferocytosis contributes to pain progression from the perspective of defective and inefficient efferocytosis and its subsequent secondary necrocytosis, cascade inflammatory response, and the shift of phenotypic plasticity and metabolism. Additionally, we investigate the roles of newly discovered genetic alterations or modifications in biological signaling pathways in pain development and chronicity, providing insights into innovative treatment strategies that modulate efferocytosis, which are promising candidates and potential avenues for further research in pain management and prevention.

Background: Central post-stroke pain (CPSP) is a chronic neuropathic pain syndrome that develops following cerebrovascular injury and currently lacks effective treatment options. Previous research from our group has found a significant number of apoptotic cells in the thalamus of CPSP rats, and in the nervous system, the failure to promptly clear apoptotic cell debris can activate microglia, triggering a persistent neuroinflammatory response that contributes to the onset and progression of CPSP. Microglia clear apoptotic cells in the central nervous system through efferocytosis, a process that reduces neuroinflammation and promotes the reprogramming of microglia toward the M2 phenotype, which is crucial for immune defense and repair mechanisms in the central nervous system. Recent studies have shown that Liver X Receptor (3 (LXR-(3) can regulate microglial efferocytic function, reduce neuroinflammation after intracerebral hemorrhage, and promote recovery of neurological function. In this study, we explore the potential mechanism by which LXR-(3 regulates microglial efferocytosis to alleviate CPSP. Methods: Based on the single-cell sequencing dataset of human brain hemorrhage patients and thalamic tissue samples from rats with central post-stroke pain, a systematic analysis of the dynamic changes in efferocytosis and the associated neuroinflammation was conducted. To verify whether LXR-(3 regulates CPSP through efferocytosis and its potential mechanism, rats were treated with GW3965 (LXR-(3 agonist), GSK2033 (LXR-(3 inhibitor), and AS1517499 (STAT6 inhibitor), either separately or in combination. Assessments included nociceptive behavior, efferocytosis, and the expression of efferocytosis-related molecules, inflammatory factors and microglial polarization markers. In vitro experiments using BV2 cells were also performed to further elucidate the underlying mechanisms. Results: Human brain hemorrhage sequencing and the CPSP rat thalamic hemorrhage model results indicated that insufficient clearance of apoptotic cells and abnormal activation of microglia were key factors contributing to abnormal neuroinflammation following a stroke. The down-regulation of LXR-(3 is associated with mechanical allodynia after CPSP. Activation of LXR-(3 enhanced efferocytosis, and upregulated efferocytosis-related molecules (MerTK, Axl, and CD36). These effects contributed to reduced neuroinflammation, promoted microglial polarization toward the M2 phenotype, and alleviated CPSP. Biological analyses and experimental results indicated that LXR-(3 regulated these effects through the activation of p-STAT6. In vitro studies also confirmed that the LXR-(3/p-STAT6 signaling pathway is closely associated with efferocytosis and inflammation regulation in BV2 cells. Conclusions: LXR-(3 promotes microglial efferocytosis and the expression of efferocytosis-related molecules (Mertk, Axl, and CD36) by activating p-STAT6, thereby reducing neuroinflammation, reprogramming microglia toward the M2 phenotype, and alleviating CPSP. Targeting LXR-(3 or its downstream signaling pathways may offer a promising therapeutic strategy for central neuropathic pain.

BACKGROUND:Central post-stroke pain (CPSP) is a chronic neuropathic pain syndrome that develops following cerebrovascular injury and currently lacks effective treatment options. Previous research from our group has found a significant number of apoptotic cells in the thalamus of CPSP rats, and in the nervous system, the failure to promptly clear apoptotic cell debris can activate microglia, triggering a persistent neuroinflammatory response that contributes to the onset and progression of CPSP. Microglia clear apoptotic cells in the central nervous system through efferocytosis, a process that reduces neuroinflammation and promotes the reprogramming of microglia toward the M2 phenotype, which is crucial for immune defense and repair mechanisms in the central nervous system. Recent studies have shown that Liver X Receptor β (LXR-β) can regulate microglial efferocytic function, reduce neuroinflammation after intracerebral hemorrhage, and promote recovery of neurological function. In this study, we explore the potential mechanism by which LXR-β regulates microglial efferocytosis to alleviate CPSP. METHODS:Based on the single-cell sequencing dataset of human brain hemorrhage patients and thalamic tissue samples from rats with central post-stroke pain, a systematic analysis of the dynamic changes in efferocytosis and the associated neuroinflammation was conducted. To verify whether LXR-β regulates CPSP through efferocytosis and its potential mechanism, rats were treated with GW3965 (LXR-β agonist), GSK2033 (LXR-β inhibitor), and AS1517499 (STAT6 inhibitor), either separately or in combination. Assessments included nociceptive behavior, efferocytosis, and the expression of efferocytosis-related molecules, inflammatory factors and microglial polarization markers. In vitro experiments using BV2 cells were also performed to further elucidate the underlying mechanisms. RESULTS:Human brain hemorrhage sequencing and the CPSP rat thalamic hemorrhage model results indicated that insufficient clearance of apoptotic cells and abnormal activation of microglia were key factors contributing to abnormal neuroinflammation following a stroke. The down-regulation of LXR-β is associated with mechanical allodynia after CPSP. Activation of LXR-β enhanced efferocytosis, and upregulated efferocytosis-related molecules (MerTK, Axl, and CD36). These effects contributed to reduced neuroinflammation, promoted microglial polarization toward the M2 phenotype, and alleviated CPSP. Biological analyses and experimental results indicated that LXR-β regulated these effects through the activation of p-STAT6. In vitro studies also confirmed that the LXR-β/p-STAT6 signaling pathway is closely associated with efferocytosis and inflammation regulation in BV2 cells. CONCLUSIONS:LXR-β promotes microglial efferocytosis and the expression of efferocytosis-related molecules (Mertk, Axl, and CD36) by activating p-STAT6, thereby reducing neuroinflammation, reprogramming microglia toward the M2 phenotype, and alleviating CPSP. Targeting LXR-β or its downstream signaling pathways may offer a promising therapeutic strategy for central neuropathic pain.

BACKGROUND:Chronic postoperative pain (CPSP) is a significant public health issue due to the complex pathophysiological mechanism. Existing evidence has pointed out that the loss of gamma-aminobutyric acid-ergic (GABAergic) neurons played a critical role in various neuropathic pain models. Previous studies also found that pyroptosis-mediated neuroinflammation was involved in neuropathological pain. However, it remains unclear what the relationship is between pyroptosis and the loss of spinal GABAergic neurons in CPSP. This study aimed to investigate the role and mechanism of GABAergic neuron pyroptosis in CPSP. METHODS:We used skin/muscle incision and retraction (SMIR) to establish the CPSP model in rats. Mechanical allodynia was assessed using the Von Frey test. Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), immunofluorescence, biochemical assay, and transmission electron microscope (TEM) were employed to investigate the role and mechanism of GABAergic neuron pyroptosis during CPSP. RESULTS:We observed the pyroptosis of GABAergic neurons in the spinal cord following SMIR. Intrathecal administration of the GSDMD inhibitor decreased the pyroptosis of GABAergic neurons in the spinal cord and reversed SMIR-induced mechanical allodynia. In addition, we found that SMIR induced a significant decrease in the level of Mfn2 in the neurons, accompanied by mitochondrial dysfunction and reactive oxygen species (ROS) accumulation in SMIR rats. Intrathecal injection of the Mfn2 activator reduced mitochondrial dysfunction and ROS, alleviated the pyroptosis of GABAergic neurons in the spinal cord, which alleviated the SMIR-induced mechanical allodynia. CONCLUSIONS:Our study demonstrated that downregulation of Mfn2 leads to mitochondrial dysfunction and ROS accumulation, which promotes the pyroptosis of spinal GABAergic neurons and the development of chronic pain.

Chronic pain (CP) affects over 30 % of the global population, imposing significant financial burdens on individuals and society. However, existing treatments for CP offer limited efficacy and troublesome side effects, primarily owing to a lack of knowledge of its precise underlying mechanism. Pathological stimuli disrupt the intricate process of protein folding and endoplasmic reticulum (ER) homeostasis. This disruption leads to the accumulation of misfolded or unfolded proteins in the ER, generating a condition termed ER stress. Emerging data have indicated that ER stress, occurring in the peripheral and central nervous systems, contributes to the development and maintenance of CP. This review aimed to comprehensively explore the intersection of ER stress and CP within the lower and upper nervous systems and highlight the cell-specific contributions of the unfolded protein response in different CP types. We provide a comprehensive synthesis of evidence from animal models, examining neuronal and non-neuronal mechanisms and discuss the damaging ER stress-linked inflammation, autophagy, oxidative stress, and apoptosis, which collectively drive disease progression and contribute to a neurotoxic environment. However, the mechanisms through which ER stress influences the most advanced centre-of-pain projections in the brain remain unclear. Further investigation in this area is crucial to elucidate the relationship between ER stress and CP and facilitate the development of novel therapeutic drugs for this intractable dilemma.

The paper studies a presynchronization control of grid connection for large merchant marine microgrid inverters. We present a virtual synchronous generator (VSG) algorithm with model-free adaptive control (MFAC) to optimize the stable grid connection of ship microgrid and shore-to-ship power. To solve poor precision of presynchronization control under nonideal ship microgrid condition, an MFAC controller and its presynchronization method are developed for grid connection of ship-distributed generation inverters. The proposed presynchronization control method effectively avoids a high transient overcurrent and achieves a seamless grid connection to different types of shore power. The simulation results verify the effectiveness of the proposed control method.

Abstract Background High doses of long-acting opioids were used to facilitate off-pump coronary artery bypass grafting procedure, which may result in opioid-related adverse events after surgery. Transcutaneous electrical acupoint stimulation (TEAS) had been reported to be effective in reducing intraoperative opioids consumption during surgery. The aim of this study is to assess whether TEAS with difference acupoints can reduce the doses of opioid analgesics. Methods This was a multicenter, randomized, controlled, double-blind trial. Patients underwent off-pump coronary artery bypass grafting under general anesthesia were enrolled. Eligible patients were randomly and equally grouped into sham acupuncture group (n = 105), regional acupoints combination group (n = 105), or distal–proximal acupoints combination group (n = 105) using a centralized computer-generated randomization system. Transcutaneous electrical acupoint stimulation was applied for 30 min before anesthesia induction. The primary outcome was the doses of sufentanil during anesthesia. Secondary outcomes included the highest postoperative vasoactive-inotropic scores within 24 h, intraoperative propofol consumption, length of mechanical ventilation, duration of cardiac care unit and postoperative hospital stay, incidence of postoperative complications, and mortality within 30 days after surgery. Results Of the 315 randomized patients, 313 completed the trial. In the modified intention-to-treat analysis, the doses of sufentanil were 303.9 (10.8) μg in the distal–proximal acupoints group, significantly lower than the sham group, and the mean difference was − 34.9 (− 64.9 to − 4.9) μg, p = 0.023. The consumption of sufentanil was lower in distal–proximal group than regional group (303.9 vs. 339.5), and mean difference was − 35.5 (− 65.6 to − 5.5) μg, p = 0.020. The distal–proximal group showed 10% reduction in opioids consumption comparing to both regional and sham groups. Secondary outcomes were comparable among three groups. Conclusion Transcutaneous electrical acupoint stimulation with distal–proximal acupoints combination, compared to regional acupoints combination and sham acupuncture, significantly reduced sufentanil consumption in patients who underwent off-pump coronary artery bypass grafting surgery.

Chronic postsurgical pain (CPSP) is increasingly recognized as a public health issue. Recent studies indicated the innate immune pathway of cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) was involved in pain regulation. However, the detailed mechanisms remain unclear. Previous studies found A1 reactive astrocytes in the spinal cord contributed to CPSP. This study aimed to investigate the roles and mechanisms of the cGAS-STING pathway in regulating the generation of A1 reactive astrocytes during CPSP. First, CPSP model was established using skin/muscle incision and retraction (SMIR) in rats. We found that cGAS-STING pathway was activated accompanied with an increase in mitochondrial DNA in the cytosol in the spinal cord following SMIR. Second, a STING inhibitor C-176 was intrathecally administrated. We found that C-176 decreased the expression of type I interferons and A1 reactive astrocytes in the spinal cord, and alleviated mechanical allodynia in SMIR rats. Third, cyclosporin A as a mitochondrial permeability transition pore blocker was intrathecally administrated. We found that cyclosporin A decreased the leakage of mitochondrial DNA and inhibited the activation of cGAS-STING pathway. Compared with C-176, cyclosporin A exhibits similar analgesic effects. The expression of type I interferons and A1 reactive astrocytes in the spinal cord were also down-regulated after intervention with cyclosporin A. Moreover, simultaneous administration of cyclosporin A and C-176 did not show synergistic effects in SMIR rats. Therefore, our study demonstrated that the cGAS-STING pathway activated by the leakage of mitochondrial DNA contributed to chronic postsurgical pain by inducing type I interferons and A1 reactive astrocytes in the spinal cord.

A multi-motor speed synchronization control method is proposed for the prefabricated vegetable vortex cleaning line in this paper. The focus of this method is to enhance the system's synchronization performance, disturbance rejection capability, dynamic response, and stability of the motors. This method is based on Model-Free Sliding Mode Control (MFSMC) combined with an enhanced deviation coupling control structure. Its objective is to tackle the challenges arising from significant variations in motor speed tracking errors, notable differences in speed and acceleration, and the complex system structure that results in unstable cleaning effects. Initially, Permanent Magnet Synchronous Motors (PMSM) are selected as the controlled objects. An improved sliding mode manifold function is introduced to minimize the rate of change in motor speed tracking errors. Utilizing this, a data-driven model-free control technique is employed to design a model-free adaptive sliding mode controller for the motors. Additionally, the deviation coupling structure is enhanced to mitigate the negative effects caused by notable differences in speed and acceleration, along with the complex system structure on the synchronization performance. Finally, a simulation analysis is performed employing three motors to evaluate the effectiveness of the offered control method. The results obtained demonstrate the superior performance of motors controlled by the proposed control method exhibit enhanced response speed, reduced overshoot, improved disturbance rejection capability, and superior speed synchronization performance.

To mitigate the impact of lateral deviation in the trajectory control of aquaculture vessels, an improve ILOS guidance law is proposed. Addressing complex sea conditions, unstable weather scenarios, and uncertainties in load, a model-free adaptive learning control (MFALC) method for aquaculture vessel heading control is introduced. Firstly, by incorporating the actual vessel position, desired trajectory, and the improved ILOS guidance law, the desired heading is obtained, and a dynamic linearization model is established solely based on input-output data. Secondly, a Pseudo-Partial Derivative (PPD) estimation algorithm is presented. Subsequently, the MFALC control is designed in conjunction with the PPD algorithm. Finally, the superiority of the proposed control method over traditional PID control is validated through simulations. Simulation results demonstrate that the proposed control method enables rapid and stable trajectory control for aquaculture vessels.

To optimize photovoltaic (PV) power generation efficiency and the stability of output power, the paper presents an MPPT (Maximum Power Point Tracking) technology for PV system of merchant marines. For the unstable weather, ship roll and the sea salt crystallization on solar panels under complex sea condition disturbance, the MPPT controller is difficult to design according to the accurate PV panels model. We propose a boost converter control strategy based on MFALC (Model Free Adaptive-learning Control). Firstly, a general discrete non-linear system is established according to the data of PV panels output and inputs; Secondly, a data model based on compact form dynamic linearization is carried out to design the MFALC controller; Thirdly, the pseudo partial derivative estimation algorithm is given. The proposed strategy effectively reduces the power oscillation of ship PV system and achieve MPPT rapidly under different operating conditions. The simulation results verify the effectiveness and advantages of the proposed control strategy compared with the perturbation and observation method.

BACKGROUND:Simulation-based training is used to improve fiberoptic bronchoscopic skills for novices. We developed a nonanatomical task trainer (named 12-hole clock model) that focused on training manipulation of bronchoscopes. The aim of this study was to evaluate the training effect of this model on bronchoscopic skills and learning interests in simulated normal and difficult airways among anesthesia residents. METHODS:Forty-three anesthesia residents without experience in bronchoscopic intubation were randomly divided into control (n = 22) and intervention groups (n = 21). All participants received standard multimedia learning and a baseline test using a normal airway manikin. Then, the control and intervention groups engaged in 60 minutes of training via a traditional airway manikin or the clock model, respectively. After training, the participants completed bronchoscopic performance assessments in simulated normal and difficult airways, as well as an electronic questionnaire related to the course. RESULTS:During training, the total hands-on time of bronchoscopic practice recorded by trainees' themselves was longer in the intervention group than in the control group (1568 ± 478 seconds vs 497 ± 172 s, P < .0001). Posttraining, the time required to visualize the carina in simulated normal airways was longer in the intervention group than in the control group (22.0 [18.0, 29.0] vs 14.0 [10.8, 18.3], P < .0001), while it was shorter for simulated difficult airways (24.0 [16.0, 32.0] s vs 27.0 [21.0, 35.5] s, P = .0425). The survey results indicated that confidence in bronchoscopic intubation increased in both groups, without significant differences in satisfaction, acceptance, or perceived difficulty between the groups. However, the interest ratings were higher in the intervention group than in the control group. CONCLUSIONS:The 12-hole clock model is a simple and feasible method for improving bronchoscopic skills and promoting interest among trainees. TRIAL REGISTRATION:NCT05327842 at Clinicaltrials.gov.

目的:观察与比较瑞马唑仑、丙泊酚单用及合用在经内镜逆行胰胆管造影术(ERCP)麻醉中的效果及安全性.方法:择期行ERCP治疗的120例患者按随机数字表分为丙泊酚组(P组)、瑞马唑仑组(R组)、瑞马唑仑联合丙泊酚组(RP组),每组各40例,3组按指定的用药方案(P组用丙泊酚;R组用瑞马唑仑;RP组瑞马唑仑联合丙泊酚)完成麻醉.比较3组患者的一般资料、手术时间和苏醒时间及麻醉前(T0)、麻醉后(T1),置镜时(T2)、十二指肠乳头切开(T3)、支架或鼻胆管置入(T4)的血氧饱和度(SpO2)、心率(HR)、平均动脉压(MAP)、呼吸频率(RR)、脑电双频指数(BIS),Ramsay镇静评分;记录与比较术中加药总次数,体动、肠蠕动过快人次数;呼吸、心血管相关不良事件和麻醉相关的术后并发症.结果:3组患者一般资料、手术时间、苏醒时间,Ramsay镇静评分,手术医师、患者满意度及麻醉相关的术后并发症发生率差异无统计学意义(P>0.05);与P组比较,R组和RP组注射痛、低血压、心动过缓和呼吸抑制、胆心反射发生率低;麻醉后RR及BIS值高,差异有统计学意义(P＜0.05).与R组比较,P组和RP组加药总次数、体动和肠蠕动过快人次数少,差异有统计学意义(P＜0.05).结论:瑞马唑仑联合丙泊酚用于ERCP麻醉效果可,过程平稳,不良反应少,值得在临床推广应用.

Pain is a common clinical condition. However, the mechanisms underlying pain are not yet fully understood. It is known that the neuroimmune system plays a critical role in the pathogenesis of pain. Recent studies indicated that the cyclic-GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway can activate the innate immune system by sensing both extrinsic and intrinsic double-stranded DNA in the cytoplasm, which is involved in pain processing. In this review, we summarise (1) the roles of the cGAS-STING pathway in different pain models, (2) the effect of the cGAS-STING pathway in different cells during pain regulation, and (3) the downstream molecular mechanisms of the cGAS-STING pathway in pain regulation. This review provides evidence that the cGAS-STING pathway has pro- and anti-nociceptive effects in pain models. It has different functions in neuron, microglia, macrophage, and T cells. Its downstream molecules include IFN-I, NF-κB, NLRP3, and eIF2α. The bidirectional roles of the cGAS-STING pathway in pain processing are mediated by regulating nociceptive neuronal sensitivity and neuroinflammatory responses. However, their effects in special brain regions, activation of astrocytes, and the different phases of pain require further exploration.

上呼吸道出血是一种临床急症,其发生突然、进展迅速,是导致气道相关性死亡的重要原因.与其他部位的出血不同,上呼吸道出血可能迅速淹没气道,导致窒息,甚至危及生命.上呼吸道出血时,因血液阻碍了气道视野,很多传统的气道管理设备的使用受到限制,为麻醉管理增加了难度.本文通过总结上呼吸道出血的常见原因、气道管理的挑战、气道管理方法,为麻醉科医师应对此类情况提供参考,从而更好地保障患者生命安全.

本文针对具有参数不确定和外负载扰动的不确定受扰电液伺服系统,提出了一种智能自学习PID控制策略.该方法不依赖于系统的精确模型,是一种数据驱动的控制方法.首先,通过改进的动态线性化方法将非线性非仿射的电液伺服系统等效为含有时变参数项和非线性不确定项的线性仿射形式;然后,采用梯度估计算法和时间差分算法分别对时变参数项和非线性不确定项进行估计;进而,利用iPID控制引入附加误差信息对过度线性化丢失的信息进行补偿;最后,根据最优准则,设计不确定受扰电液伺服系统的参数更新律和学习控制律.本文通过理论分析与仿真实验验证了该控制策略的收敛性,并通过对比实验,验证了该控制方案应用于电液伺服系统的优越性和精确性.该控制方法抑制了非线性扰动对系统造成的不良影响,并能实现理想轨迹的精确跟踪.