Search

Male spermatogenesis dysfunctions are associated with environmental pollutants, but the detailed mechanisms remain poorly understood. In this study, healthy C57BL/6 J mice were used to establish an animal model of maternal exposure to traffic pollutant during pregnancy, and the toxic effects on the reproductive system of F2 male mice were analysed using mRNA and miRNA microarray. Our results showed that 54 miRNAs and 1927 mRNAs were significantly altered in the exposed group. Gene Ontology (GO) analysis revealed that the most significant GO terms for biological process, molecular function and cellular component were myeloid cell differentiation, growth factor binding and main axon. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis demonstrated that the biosynthesis of amino acids was the most significant pathway and that the cytokine-cytokine receptor interaction was the most abundant pathway (37 genes). Protein-protein interaction (PPI) and the miRNA-mRNA network were constructed with Cytoscape. The hub genes, Tnf, Il10 and Gapdh, were closely related to immuno-regulation and their miRNA regulators were reversely changed. Together, our results indicate that maternal exposure to traffic pollutant can cause spermatogenesis damage in F2 male mice possibly through the destroyed immunoprivileged environment in testis mediated by the aberrant expression of miRNA and mRNA.

Ethylparaben (EtP) and propylparaben (PrP) are common preservatives and well-known endocrine-disrupting chemicals. Studies have demonstrated that they can reduce female fertility, but the underlying mechanism, especially that on embryo implantation, is still poorly understood. Endometrial decidualization is a critical event for embryo implantation. In this study, we aimed to explore the effects of EtP/PrP on endometrial decidualization. Pregnant mice were dosed daily by oral gavage with EtP at 0, 400, 800 and 1600 mg/kg or with PrP at 0, 625, 1250 and 2500 mg/kg from Day 1 of pregnancy until sacrifice. The results showed that the rate of pregnant mice with impaired embryo implantation, whose number of implantation sites was less than 7, was significantly increased after exposure to 1600 mg/kg EtP or 2500 mg/kg PrP. Further study found that the expression of endometrial decidualization markers HOXA10, MMP9 and PR was significantly downregulated in 1600 mg/kg EtP group and 2500 mg/kg PrP group. Notably, serum oestrogen and progesterone levels were significantly increased, whereas the expression of uterine oestrogen receptor and progesterone receptor was decreased following 1600 mg/kg EtP or 2500 mg/kg PrP exposure. In the breeding test, fewer offspring were found after females were exposed to 1600 mg/kg EtP or 2500 mg/kg PrP in early pregnancy. This demonstrated that exposure to EtP/PrP interfered with embryo implantation by compromising endometrial decidualization in early-stage pregnant mice. Disorders of reproductive hormones and hormone receptor signals could be responsible for impaired decidualization. This study broadened the understanding on the biological safety of EtP and PrP.

Decidualization accompanies with extensive stromal cell proliferation and differentiation, is a crucial step in early pregnancy. Aberrant decidualization is linked to infertility and miscarriage but the mechanisms remain unclear. Carnitine palmitoyltransferase 1A (CPT1A) is an enzyme catalyzing key steps in the fatty acid beta-oxidation pathway. The objective of this study was to investigate the role of CPT1A in decidualization during early pregnancy. An increased expression of CPT1A was found both in Days 6 and 7 as compared with in Days 1, 4 and 5. Further examination showed that on days 5–7 of pregnancy, the protein level of CPT1A was strongly up-regulated at implantation sites compared with inter-implantation sites, the location of CPT1A protein was distributed in the decidual zone. Upon further exploration, CPT1A expression was significantly increased in response to artificially induced decidualization both in vivo and in vitro. After down-regulating CPT1A expression by CPT1A-small interfering RNA (siCPT1A) in primary mouse endometrial stromal cells, expressions of decidualization markers and cell proliferation markers were decreased. After siCPT1A was transfected into the mouse uterus, decidualization impaired and then led to the loss of the implanted embryos. Thus, CPT1A is important for decidualization in mice and it may regulate the stromal cell proliferation progress. It is worth noting that the expression of CPT1A protein of human decidua was significantly decreased in spontaneous abortion groups compared to normal pregnancy groups. Collectively, CPT1A is essential for endometrium of early pregnant mice and humans.

Ferroptosis is a novel iron-dependent form of cell death implicated in brain pathology. However, whether arsenite is an inducer of ferroptosis in the neuron remains completely unknown. In this study, the seven-week-old healthy C57BL/6 J male mice were treated with environmental related doses (0.5, 5 and 50 mg/L) of arsenite for 6 months via drinking water, and the ferroptosis-related indicators were further determined. Our results demonstrated for the first time that, arsenite exposure significantly reduced the number of neuron and caused the pathological changes of mitochondria in the cerebral cortex of mice. We further revealed that arsenite induced ferroptotic cell death in neuron by accumulation of reactive oxygen species and lipid peroxidation products, disruption of Fe2+ homeostasis, depletion of glutathione and adenosine triphosphate, inhibition of cysteine/glutamate antiporter, activation of mitogen-activated protein kinases and mitochondrial voltage-dependent anion channels pathways, up-regulation of endoplasmic reticulum stress, all of which were involved in the process of ferroptosis. These findings were also verified in the cultured PC-12 cells by using ferropotosis inhibitor, desferoxamine. Taken together, our results not only reveal a novel mechanism that chronic arsenite exposure may trigger the new form of cell death, ferroptosis, but also shed a new light on a potential clue for the intervention and prevention against arsenite-related neurodegenerative diseases.

Arsenite exposure is known to increase the risk of neurological disorders via alteration of dopamine content, but the detailed molecular mechanisms remain largely unknown. In this study, using both dopaminergic neurons of the PC-12 cell line and C57BL/6J mice as in vitro and in vivo models, our results demonstrated that 6 months of arsenite exposure via drinking water caused significant learning and memory impairment, anxiety-like behavior and alterations in conditioned avoidance and escape responses in male adult mice. We also were the first to reveal that the reduction in dopamine content induced by arsenite mainly resulted from deficits in dopaminergic neurotransmission in the synaptic cleft. The reversible N6- methyladenosine (m6A) modification is a novel epigenetic marker with broad roles in fundamental biological processes. We further evaluated the effect of arsenite on the m6A modification and tested if regulation of the m6A modification by demethylase fat mass and obesity-associated (FTO) could affect dopaminergic neurotransmission. Our data demonstrated for the first time that arsenite remarkably increased m6A modification, and FTO possessed the ability to alleviate the deficits in dopaminergic neurotransmission in response to arsenite exposure. Our findings not only provide valuable insight into the molecular neurotoxic pathogenesis of arsenite exposure, but are also the first evidence that regulation of FTO may be considered as a novel strategy for the prevention of arsenite-associated neurological disorders.

Benzo[a]pyrene (B[a]P), a ubiquitous chemical contaminant in the environment, is a well-established neurotoxicant to human. However, the molecular mechanisms for B[a]P neurotoxicity are still unclear. In the present study, after treating Sprague-Dawley rats with 0.02, 0.2 and 2.0mg/kg/day B[a]P for 7 weeks [from postnatal day (PND) 5 to PND54], our results showed that B[a]P exposure caused a significant deficits in learning and memory function. By using U87 cells as in vitro model, the significant cytotoxicity and the induction of apoptosis caused by B[a]P were further verified. More importantly, we demonstrated for the first time that B[a]P exposure caused the disruption of glutamate (Glu) neurotransmitter transmission by decreasing the level of Glu, reducing the expression of Glu receptors (GluR1 and GluR2), enhancing the level of SNAP-25, widening the synaptic cleft, and ultimately producing the neurotoxic effects in both cells and animals. Our results will provide novel evidence to reveal the possible role of SNAP-25 in B[a]P-induced neurotoxicity and may be helpful for searching the potential strategy for the prevention measures against B[a]P neurotoxicity.

Objective: To evaluate the effects of occupational exposures to coke oven emissions (COEs) and benzo[a]pyrene (B[a]P) on the prevalence of hypertension and abnormal electrocardiogram (ECG) in coke oven workers. Methods: We included 880 coke oven workers and 710 oxygen employees in the exposed and control groups, respectively. Blood pressure (BP), ECG, blood lipid levels, and glucose levels of all subjects were measured. COE and B[a]P concentrations at the bottom, side, and top of the oven and control plants were estimated by weighing and high-performance liquid chromatography. Results: The COE concentration at the top and side was higher than that at the bottom (P < 0.05). The levels of B[a]P at the top and side significantly exceeded the limit value. Abnormal BP, ECG, the detection ratio of hypertension and left ventricular high voltage were significantly greater in the exposed group than in the control group (P < 0.05). The logistic regression analysis results revealed that age and B[a]P exposure were risk factors for hypertension in coke oven workers (P < 0.05) and both were risk factors for abnormal ECG (P < 0.05). Moreover, B[a]P exposure, age, and gender were risk factors for impaired fasting glucose in coke oven workers (P < 0.05). Conclusions: B[a]P and COE exposures are risk factors for hypertension and abnormal ECG in coke oven workers.

Benzo[a]pyrene (B[a]P) is a ubiquitous neurotoxic pollutant that widely distributes in the natural environment. However, the exact mechanism of B[a]P-induced neurotoxicity has not been well established. As one key synaptic protein, SNAP-25 plays an important role in the regulation of neurotransmitter release, including synaptic dopamine release. In this study, we demonstrated that, after intragastric administration of B[a]P in rats aged postnatal day 5 for 7 weeks, B[a]P significantly increased the level of dopamine and the expression of SNAP-25, dopamine receptor 1 (DRD1) and DRD 3. Moreover, treatment of B[a]P also caused the ultra-structural pathological changes in the cerebral cortex of rats. To further reveal the potential role of SNAP-25 in the regulation of DRDs, we treated the dopaminergic PC-12 cells with 20 μM B[a]P for 24 h. A significant cytotoxicity and apoptosis were observed, and more importantly, we found that SNAP-25, DRD 1 and DRD 3 co-localized in the cells, and down-regulation of SNAP-25 by CRISPR-Cas9 plasmid remarkably reduced the expression of DRD1 and DRD3. Together, our findings suggest that, synaptic dopamine release may be positively regulated by SNAP-25 via its receptors, and thus affecting the neurotoxicity induced by B[a]P.

The authors describe a colorimetric method for the determination of the staphylococcal enterotoxin B (SEB) that also allows for visual readout. The assay is based on the growth of gold nanoparticles (AuNPs) mediated by a hemin/G-quadruplex DNAzyme which generates a color change from red to blue in the presence of SEB. The method is enzyme-free and does not require a label. The kinetics of the formation of the AuNPs is controlled by the hemin/G-quadruplex DNAzyme and this is key to the signal generation mechanism. In the presence of SEB, the reactions between aptamer and target modulated the amount of single probe G strands that form DNAzyme capable of consuming hydrogen peroxide. The growth process of AuNPs is influenced by the resulting concentration of H2O2 and leads to the color change. Under optimal conditions, a linear relationship exists between absorbance and SEB concentration in the range from 0.1 to 500 pg·mL‾1 which covers the clinically relevant range. In case of visual detection, the lower limit of detection is 1 pg·mL−1. The assay described here is sensitive, comparably inexpensive and can detect SEB rapidly without the need for sophisticated equipment. In our perception, the method has a wide scope in that it may be adapted to various nucleic acids, proteins and other biomolecules if respective aptamers are available.

Ferroptosis is a newly identified form of cell death characterized by accumulation of intracellular iron and requirement of lipid peroxidation. However, whether arsenite triggers testicular cell death via ferroptosis remains unclear. In this study, after administrating of adult male mice with 0.5, 5 and 50 mg/L arsenite for six months via drinking water, the results showed that arsenite caused the pathological changes in mouse testis and significantly reduced the number of sperm. Mitochondrial injuries were observed as the major ultrastructural damages induced by arsenite, and these damages were accompanied by the apparent mitochondrial oxidative damage in the testis, manifested by accumulation of iron, production of reactive oxygen species and lipid peroxidation products. We also demonstrated that arsenite significantly activated ferroptosis-related signal pathways in the mouse testis. To further verify the results obtained in the animal model, GC-2spd cells were employed as the in vitro culture system. Consistently, the results revealed arsenite remarkably triggered the ferroptotic cell death in vitro, and inhibition of ferroptosis by ferrostatin-1 could attenuate this adverse effect in cells. These findings together indicate that arsenite can trigger oxidative stress thus leading to testicular cell death by ferroptosis, suggesting that inhibition of ferroptosis would be a potential strategy for treatment of arsenite-related male reproductive toxicity.

We describe a turn-on electrochemical biosensor for the detection of methyltransferases (MTases) causing DNA adenine methylation. This biosensor is based on insertion, methylation-resistant cleavage, signal enrichment caused by gold nanoparticles (AuNPs), and a signal probe-dragging strategy. A double-stranded DNA (dsDNA) containing identical MTase and methylation-resistant endonuclease (Mbo I) sites was immobilized on the surface of a gold electrode via Au-S covalent binding. The surface was subsequently treated with MTase and Mbo I and then washed. Results revealed that the surface of the electrode contains methylated dsDNA and 12-base nucleotides residual. Depending on biotin-streptavidin interactions that enabled signal probes and nucleotide residue hybridization and AuNP enrichment, a large number of signal probes labeled with ferrocene (Fc) are captured by the electrode. Under optimal conditions, the differential pulse voltammetry signals of Fc tags (at a working voltage of 0.24 V vs. Ag/AgCl) are linearly related to the log of the MTase activity in the 0.1 to 40 U·mL−1 range. The dynamic range extends from 0.05 to 50 U·mL−1, and the limit of detection is 0.024 U·mL−1 (at an S/N ratio of 3). The assay is well reproducible and highly selective. In our perception, this strategy provides a promising approach for simple, sensitive and selective detection of Dam MTase and may be extended to the determination of other MTase by exchanging the corresponding DNA.

Objective This study aimed to assess the association between exposure to the Great Chinese Famine (1959–1961) during early life and hypertension in adulthood. Methods From July to September 2009, 1224 eligible adults were recruited in a cross-sectional survey using a multi-stage stratified random sampling method in Chongqing China. A questionnaire was used to collect information of hypertension and sociodemographic factors. Participants were categorized as childhood, fetal, and none exposure to famine based on the date of birth. Results Of the sample, 12.3% reported having hypertension. The prevalence of hypertension varied by famine status: 11.9% in childhood exposure, 16.1% in fetal exposure, and 10.2% in non-exposure group. After adjusting for sociodemographic and lifestyle factors, compared with non-exposure group, fetal exposure group had an increased likelihood of having hypertension with odds ratio of 1.79 (95%CI 1.13-2.84). Although there was no significant gender and famine interaction, the positive association between famine exposure and hypertension was stronger among women than men. Conclusion Fetal exposure to the Chinese famine may be associated with an increased risk of arthritis in adulthood in women.

Objectives To investigate whether postnatal benzo(a)pyrene (B(a)P) exposure caused the impairments on the process of neurodevelopment and the alteration in the calcium medium in the neonatal rats. Material and methods Eighty neonatal Sprague Dawley (SD) rats were randomly divided into 5 groups (untreated control group, vehicle group, 0.02 mg/kg, 0.2 mg/kg and 2 mg/kg B(a)P-exposed group). Rats were treated with B(a)P by the intragastric administration from postnatal day (PND) 4 to 25. Morris water maze (MWM) was employed to observe the spatial memory of rats. The activity of calcium adenosine triphosphatase (Ca2+-ATPase), sodium-potassium adenosine triphosphatase (Na+-K+-ATPase) and calcium-magnesium adenosine triphosphatase (Ca2+-Mg2+-ATPase) in the hippocampus were detected by commercial kits. Fura-2 pentakis(acetoxymethyl) (Fura-2/AM) probe and reactive oxygen species (ROS) reagent kit were used for measuring the concentration of Ca2+ and ROS in the hippocampus synapse, respectively. Results Rats exposed to B(a)P resulted in the deficits in the spatial memory manifested by the increased escape latency and decreased number of crossing platform and time spent in target quadrant in comparison with the control groups. Benzo(a)pyrene exposure caused the significant decrease in the ATPase activity in the hippocampus and caused Ca2+ overload in the synaptic, besides, the ROS concentration increased significantly which may further induce neurobehavioral impairment of the neonatal rats. Conclusions Our findings suggest that postnatal B(a)P exposure may cause the neurobehavioral impairments in the neonatal rats, which were mediated by the decreased ATPase activity and elevated Ca2+ concentration. Int J Occup Med Environ Health 2017;30(2):203-211.

An ultrasensitive and specific electrochemical biosensor for the determination of mecA gene, which is associated with methicillin resistant strains, was successfully developed. Capture probes were immobilized on the surface of a gold nanoparticle modified glassy carbon electrode. After target probes were hybridized with capture probes, dual labeled gold nanoparticles with alkaline phosphatase and detection probes were hybridized with target probes for sensitive detection of mecA gene fragments. Dual labeled gold nanoparticles, which acted as a high-efficiency signal amplification strategy, were successfully prepared. The gold nanoparticles and dual labeled gold nanoparticles were characterized by transmission electron microscopy. Different concentrations of gene fragments were detected to inspect the specificity and sensitivity of the proposed biosensor. This biosensor displayed outstanding selectivity and a remarkable sensitivity (LOD = 23 pM, S/N = 3). Good linearity over the range of 50 pM to 250 pM wa...

The ‘Conclusion’ section in the Abstract was published incorrectly in the original publication of the article [1] and is corrected with this erratum as below: “Fetal exposure to the Chinese famine may be associated with an increased risk of hypertension in adulthood in women.”

The developmental origins hypothesis postulates that under-nutrition in the early stage of life is associated with an increased risk of disease in adulthood. This study aimed to examine the association of exposure to the Chinese famine of 1959 to 1961 in early life with the risk of arthritis in adulthood. From July to September 2009, the study adopted multistage stratified random sampling cross-sectional survey to recruit 1224 eligible adults in Chongqing. Famine exposure groups were categorized into 3 groups: (1) childhood exposure, (2) fetal exposure, and (3) nonexposure. Self-reported arthritis of physician diagnosis was obtained. A total of 1224 eligible respondents were interviewed, including 299 individuals exposed during childhood, 455 exposed when fetal, and 470 without exposure. The prevalence of arthritis in adulthood among individuals exposed to famine during childhood was significantly higher than those not exposed (17.39% vs 11.28%, odds ratio [OR] = 1.573 with a 95% confidence interval of [CI] [1.020, 2.424]). Persons exposed to famine during the fetal period did not significantly contribute to a higher rate of arthritis in adulthood than those who were not exposed to famine (13.19% vs 11.28%, OR = 1.072, 95% CI = 0.713, 1.613). In addition, education level, the average monthly income, sleep status, and satisfaction of the present living condition were associated with the risk of arthritis in adulthood. Exposure to the Chinese famine during childhood may be associated with an increased risk of arthritis in adulthood. This study suggests that early life nutrition may have an effect on the risk of arthritis in adulthood.

Previous studies demonstrate that benzo(a)pyrene (B(a)P) can affect hippocampal function and cause spatial cognition impairment. However, the mechanism is incomplete. Some evidence implies that B(a)P may cause an oxidative damage linking to the function of the hippocampus and antioxidant can prevent the oxidative damage in rats, but the ATPase and Ca(2+) in the hippocampus and the protective effect of butylated hydroxyanisole (BHA) have not been studied. This study aimed to investigate the damage of toxicity further induced by B(a)P in hippocampus and the protective effect of BHA. Ninety-six male Sprague-Dawley (SD) rats were randomly divided into four groups (solvent control group, BHA-group, B(a)P-exposed group and B(a)P-BHA-combination group), with daily administration for 90 days. Morris water maze (MWM) was employed to evaluate the learning and memory ability. The levels of malonaldehyde (MDA) content, superoxide dismutase (SOD) activity, Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)ATPase activity in hippocampus were measured by commercial kits. The concentration of Ca(2+) in rat hippocampus was detected by fluorescent labeling. In behavior test it showed that there was an adverse effect on rats in the B(a)P -group. The levels of MDA content and Ca(2+) content were significantly increased in the B(a)P group, while the activities of SOD and ATPase were significantly decreased. In the B(a)P-BHA group, the change of each index diminished significantly. The results suggested that the neurobehavioral toxicity of B(a)P might have a close relationship with oxidative damage, resulted in decreasing of ATPase activities and increasing of Ca(2+) concentration in the hippocampus. Furthermore, BHA can prevent these damages.

In order to overcome the parameter uncertainties, enhance the fast tracking performance of PMSM servo system, a self-tuning fuzzy PI+PD controller is proposed first in this paper. The self-tuning fuzzy PI+PD controller is fast; computing on-line easily and can reduce stability error, especially fitting for application in the speed control of the PMSM servo system. Then an observer is adopted to observe load torque and the observed load torque is also feedforward through a weighting factor to compensate the load torque disturbance. To demonstrate the advantages of the fuzzy PI+PD controller and the load torque feedforword control, the simulation was executed in this research. The simulation results show that the proposed control scheme not only enhances the fast tracking performance, but also increases the robustness of the synchronous motor drive system.

In contrast to conventional flux-weakening control methods, an algorithm based on operation times (T 0 ) of zero voltage space vector for permanent magnet synchronous motor (PMSM) is proposed. In this paper, the d-axis current (i d ) is derived from a fuzzy controller. The proposed strategy can achieve fast dynamic control performance as well as parameter insensitivity in the flux-weakening region. Otherwise, it can also reduce the current amplitude of stator compared with the conventional method.

Direct torque control based on space vector modulation (SVM-DTC) preserve DTC transient merits, furthermore, produce better quality steady-state performance in a wide speed range. The SVM-DTC system based on input-output linearization technique for induction machine drives is developed in this paper. A sliding-mode observer for estimating flux is introduced. The observer is inherently sensorless because they do not employ the rotor speed adaptation, and thus they are insensitive to speed estimation errors. Moreover, the observer is extremely robust. The simulations of conventional DTC and the proposed control topologies are given and discussed. It is concluded that the proposed control topology outperforms the conventional DTC in reducing torque ripple and parameter robust.

In view of the operation characters of permanent magnet synchronous motor (PMSM) for hybrid electric vehicle (HEV) application, efficiency optimization control strategy is needed to meet the demand of rapidity. An efficiency optimized vector control scheme is presented in this paper. The initial value of d-axis current can be achieved in any constant speed and torque operating point by loss model, and optimized through the gradient search technique and the golden section technique. Results of experiments are provided to demonstrate the effectiveness of the proposed method.

In contrast to conventional flux-weakening control methods, an algorithm based on operation times (T0) of zero voltage space vector of permanent magnet synchronous motor (PMSM) for hybrid electric vehicle (HEV) application is proposed. In this paper, the d-axis current (id) is derived from a fuzzy controller. The proposed strategy can achieve fast dynamic control performance as well as parameter insensitivity in the flux-weakening region. Otherwise, it can also reduce the current amplitude of stator compared with the conventional method.

In servo motor drive applications, the variation of load inertia will degrade drive performance severely. Good dynamic and static performance of servo system requires controlling inertia robustly. In order to get the moment of rotational inertia, online identification methods based on model reference adaptive identification (MRAI) were developed in this paper. Then, a real-time IP position controller based on identified inertia is designed by neural network for permanent magnet synchronous motor (PMSM) servo system. The neural networks configuration is simple and reasonable, and the weight has definitely physical meaning. It has rapidly adjusting character to realize the real-time control. To demonstrate the advantages of the proposed real-time IP control scheme based on neural network, the simulation was executed in this research. The simulation results show that the proposed control scheme not only enhances the fast tracking performance, but also increases the robustness of the synchronous motor drive system.

A new scheme to estimate the moment of inertia in the motor drive system in very low speed is proposed. The simple speed estimation scheme, which is used in most servo systems for low-speed operation, is sensitivity to variations in machine parameters especially the moment of inertia. To estimate the motor inertia value, an extended Luenberger observer (ELO) is applied. The observer gain matrix can be adjusted on-line based on dynamic neural network. The effectiveness of the proposed ELO is verified by simulation.

In order to deal with the uncertainties of permanent magnet synchronous servo motor, inertia, torque load and viscous damping coefficient are online identified based on recursive least-square (RLS) estimator simultaneously. Then, a novel self-tuning PI controller based on iteration self-learning scheme is designed. Along with the regulation process, the system can remember effective historical control experience so as to change the learning gain and speed up the time of the whole process. Once the expected output is reached, the system will log the current load torque and PI gain. A database of the matched parameter is also built. With the increasing time of tuning, the database information becomes rich. If the identified inertia, load torque and viscous damping coefficient match the database information, an ideal PI gain can be acquired immediately without the adjustment process. Result of simulations show that the self-tuning PI controller outperforms the fixed PI scheme in rise time, overshoot and precise of the output when the parameter varied.

To reduce torque ripples and improve dynamic performance, a novel implementation of neural network and multi-fuzzy controller for permanent magnet synchronous motor (PMSM) direct torque controlled (DTC) drive is presented, which replaces the conventional hystersis controller with fuzzy controller (FCI) and includes a neural network speed controller (NC). To tune the weights and biases of the neural networks online, another fuzzy controller (FC2) is adopted. It combines the capability of fuzzy reasoning in handling uncertain information and the capability of neural network in learning from processes. Results of simulation are provided to demonstrate that the proposed drive has low flux linkage and torque ripples, and has quick response performance even under the occurrence of parameter variations and external disturbance.

A novel implementation of speed controller based on adaptive fuzzy neural network controller (FNNC) for permanent magnet synchronous motor (PMSM) is presented in this paper. FNNC includes one neural network controller (NC) and two fuzzy controllers (FC). It combines the capability of fuzzy reasoning in handling uncertain information and the capability of neural network in learning from processes. The initial weights and biases of the artificial neural network (ANN) are obtained by offline training method. Using the output of one fuzzy controller (FC), online training is carried out to update the weights and biases of the ANN. To improve the dynamic performances of the PMSM drive, another fuzzy controller is adopted. Results of simulation are provided to demonstrate the effectiveness of the proposed FNNC under the occurrence of parameter variations and external disturbance.

To compensate voltage difference between the reference and the actual output voltages caused by dead-time effects, a novel compensation method for permanent magnet synchronous motor (PMSM) direct torque controlled (DTC) drive based on neuro-fuzzy observer is proposed. This method presents the implementation of a voltage distortion observer based on the artificial neural network (ANN). Using the output of the fuzzy controller (FC1), online training is carried out to update the weights and biases of the ANN. To reduce torque and flux linkage ripples, another fuzzy controller (FC2) is adopted to replace the conventional hystersis controller. The proposed control scheme combines the capability of fuzzy reasoning in handling uncertain information and the capability of neural network in learning from processes. Results of simulations and experiments are provided to demonstrate the effectiveness of the proposed method even under the occurrence of different reference speed and load torque.

In order to deal with the uncertainties of permanent magnet synchronous motor, the moment of inertia, viscous damping coefficient and load torque are online identified simultaneously based on recursive least-square (RLS) estimator, which is composed of RLS estimator and a torque observer. Then, a novel self-tuning PI controller is real-time designed according to the identified parameter based on pole assignment theory, to match the time-domain command tracking specification. The moment of inertia and viscous damping coefficient identified are used to update the parameters of the observer, so the observer can observe the load torque well and truly when the parameters of the system varied severely. Then, the observed disturbance torque is fed forward, to increase the robustness of the synchronous motor drive. The simulation results show that the method not only enhances the fast tracking performance, but also increases the robustness of the synchronous motor drive.

To compensate voltage difference between the reference and the actual output voltages caused by dead-time effects, a novel compensation method for permanent magnet synchronous motor (PMSM) drive based on neuro-fuzzy observer is proposed. This method presents the implementation of a voltage distortion observer based on the artificial neural network (ANN), using the output of the fuzzy controller (FC), online training is carried out to update the weights and biases of the ANN. It combines the capability of fuzzy reasoning in handling uncertain information and the capability of neural network in learning from processes. Results of experiments are provided to demonstrate the effectiveness of the proposed method under the occurrence of different reference speed and load torque.

This paper presents the implementation of adaptive fuzzy neural network controller (FNNC) for accurate speed control of a permanent magnet synchronous motor (PMSM). FNNC includes neural network controller (NC) and fuzzy logic controller (FC). It combines the capability of fuzzy reasoning in handling uncertain information and the capability of neural network in learning from processes. The initial weights and biases of the artificial neural network (ANN) are obtained by offline training method. Using the output of the fuzzy controller (FC), online training is carried out to update the weights and biases of the ANN. Several results of simulation and experiment are provided to demonstrate the effectiveness of the proposed FNNC under the occurrence of parameter variations and external disturbance.

For permanent magnet synchronous motor (PMSM) direct torque controlled (DTC) drive, stator resistance variation and conventional hysteresis controller will bring high flux linkage and torque ripples inevitably. In order to solve this problem, the implementation of fuzzy direct torque controlled drive for permanent magnet synchronous based on neural networks is presented, which replaces the conventional hysteresis controller with fuzzy controller and estimates the stator resistance on line using the learning capability of neural networks. Results of simulation are provided to demonstrate that the proposed drive has low flux linkage and torque ripples, and has the quick response performance even under the occurrence of parameter variations and external disturbance.

This paper presents the implementation of adaptive fuzzy neural network controller (FNNC) for accurate speed control of a permanent magnet synchronous motor (PMSM). FNNC includes neural network controller (NC) and fuzzy logic controller (FC). It combines the capability of fuzzy reasoning in handling uncertain information and the capability of neural network in learning from processes. The initial weights and biases of the artificial neural network (ANN) are obtained by offline training method. Using the output of the fuzzy controller (FC), online training is carried out to update the weights and biases of the ANN. Several results of simulation are provided to demonstrate the effectiveness of the proposed FNNC under the occurrence of parameter variations and external disturbance.