Neurotoxicity Research最新文献_第8页

p-Nrf2/HO-1 Pathway Involved in Methamphetamine-induced Executive Dysfunction through Endoplasmic Reticulum Stress and Apoptosis in the Dorsal Striatum. p-Nrf2/HO-1通路通过内质网应激和后纹状体细胞凋亡参与甲基苯丙胺诱导的执行功能障碍。

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-10-01 Epub Date: 2023-05-18 DOI: 10.1007/s12640-023-00650-7

Tao Wei, Jun-Da Li, Yu-Jing Wang, Wei Zhao, Fan Duan, Yan Wang, Ling-Ling Xia, Zhao-Bin Jiang, Xun Song, Yu-Qiong Zhu, Wen-Yi Shao, Ze Wang, Kang-Sheng Bi, Hui Li, Xiao-Chu Zhang, Dong-Liang Jiao

{"title":"p-Nrf2/HO-1 Pathway Involved in Methamphetamine-induced Executive Dysfunction through Endoplasmic Reticulum Stress and Apoptosis in the Dorsal Striatum.","authors":"Tao Wei, Jun-Da Li, Yu-Jing Wang, Wei Zhao, Fan Duan, Yan Wang, Ling-Ling Xia, Zhao-Bin Jiang, Xun Song, Yu-Qiong Zhu, Wen-Yi Shao, Ze Wang, Kang-Sheng Bi, Hui Li, Xiao-Chu Zhang, Dong-Liang Jiao","doi":"10.1007/s12640-023-00650-7","DOIUrl":"10.1007/s12640-023-00650-7","url":null,"abstract":"Methamphetamine (METH) abuse is known to cause executive dysfunction. However, the molecular mechanism underlying METH induced executive dysfunction remains unclear. Go/NoGo experiment was performed in mice to evaluate METH-induced executive dysfunction. Immunoblot analysis of Nuclear factor-E2-related factor 2 (Nrf2), phosphorylated Nrf2 (p-Nrf2), heme-oxygenase-1 (HO-1), Glucose Regulated Protein 78(GRP78), C/EBP homologous protein (CHOP), Bcl-2, Bax and Caspase3 was performed to evaluate the levels of oxidative stress, endoplasmic reticulum (ER) stress and apoptosis in the dorsal striatum (Dstr). Malondialdehyde (MDA) levels and glutathione peroxidase (GSH-Px) activity was conducted to evaluate the level of oxidative stress. TUNEL staining was conducted to detect apoptotic neurons. The animal Go/NoGo testing confirmed that METH abuse impaired the inhibitory control ability of executive function. Meanwhile, METH down-regulated the expression of p-Nrf2, HO-1 and GSH-Px and activated ER stress and apoptosis in the Dstr. Microinjection of Tert-butylhydroxyquinone (TBHQ), an Nrf2 agonist, into the Dstr increased the expression of p-Nrf2, HO-1, and GSH-Px, ameliorated ER stress, apoptosis and executive dysfunction caused by METH. Our results indicated that the p-Nrf2/HO-1 pathway was potentially involved in mediating methamphetamine-induced executive dysfunction by inducing endoplasmic reticulum stress and apoptosis in the dorsal striatum.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 5","pages":"446-458"},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10281711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exercise Improves Orofacial Pain and Modifies Neuropeptide Expression in a Rat Model of Parkinson's Disease. 在帕金森病大鼠模型中，运动改善口面疼痛并改变神经肽的表达。

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-10-01 Epub Date: 2023-06-02 DOI: 10.1007/s12640-023-00651-6

Karina Henrique Binda, Marucia Chacur, Daniel Oliveira Martins

{"title":"Exercise Improves Orofacial Pain and Modifies Neuropeptide Expression in a Rat Model of Parkinson's Disease.","authors":"Karina Henrique Binda, Marucia Chacur, Daniel Oliveira Martins","doi":"10.1007/s12640-023-00651-6","DOIUrl":"10.1007/s12640-023-00651-6","url":null,"abstract":"Pain is a common non-motor symptom of Parkinson's disease (PD), which often occurs in the early disease stages. Despite the high prevalence, it remains inadequately treated. In a hemi-parkinsonian rat model, we aimed to investigate the neurochemical factors involved in orofacial pain development, with a specific focus on pain-related peptides and cannabinoid receptors. We also evaluated whether treadmill exercise could improve orofacial pain and modulate these mechanisms. Rats were unilaterally injected in the striatum with either 6-hydroxydopamine (6-OHDA) or saline. Fifteen days after stereotactic surgery, the animals were submitted to treadmill exercise (EX), or remained sedentary (SED). Pain assessment was performed before the surgical procedure and prior to each training session. Pain-related peptides, substance P (SP), calcitonin gene-related peptide (CGRP), and transient receptor potential vanilloid type 1 (TRPV1) activation and cannabinoid receptor type 1 (CB1) and type 2 (CB2) were evaluated in the trigeminal nucleus. In order to confirm the possible involvement of cannabinoid receptors, we also injected antagonists of CB1 and CB2 receptors. We confirmed the presence of orofacial pain after unilateral 6-OHDA-injection, which improved after aerobic exercise training. We also observed increased pain-related expression of SP, CGRP and TRPV1 and decreased CB1 and CB2 in the trigeminal ganglion and caudal spinal trigeminal nucleus in animals with PD, which was reversed after aerobic exercise training. In addition, we confirm the involvement of cannabinoid receptors since both antagonists decreased the nociceptive threshold of PD animals. These data suggest that aerobic exercise effectively improved the orofacial pain associated with the PD model, and may be mediated by pain-related neuropeptides and cannabinoid receptors in the trigeminal system.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 5","pages":"459-470"},"PeriodicalIF":3.7,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10228985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to: The Effects of Long-term, Low-dose β-N-methylamino-L-alanine (BMAA) Exposures in Adult SOD^G93R Transgenic Zebrafish. 更正：长期、低剂量β-N-甲基氨基-L-丙氨酸（BMAA）暴露对成年SODG93R转基因斑马鱼的影响。

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-10-01 DOI: 10.1007/s12640-023-00664-1

Ryan D Weeks, Sandra A Banack, Shaunacee Howell, Preethi Thunga, James S Metcalf, Adrian J Green, Paul A Cox, Antonio Planchart

引用次数: 0

The Effects of Long-term, Low-dose β-N-methylamino-L-alanine (BMAA) Exposures in Adult SOD^G93R Transgenic Zebrafish. 长期、低剂量β-N-甲基氨基-L-丙氨酸（BMAA）暴露对成年SODG93R转基因斑马鱼的影响。

IF 2.9 3区医学

Neurotoxicity Research Pub Date : 2023-10-01 Epub Date: 2023-08-08 DOI: 10.1007/s12640-023-00658-z

Ryan D Weeks, Sandra A Banack, Shaunacee Howell, Preethi Thunga, James S Metcalf, Adrian J Green, Paul A Cox, Antonio Planchart

{"title":"The Effects of Long-term, Low-dose β-N-methylamino-L-alanine (BMAA) Exposures in Adult SODG93R Transgenic Zebrafish.","authors":"Ryan D Weeks, Sandra A Banack, Shaunacee Howell, Preethi Thunga, James S Metcalf, Adrian J Green, Paul A Cox, Antonio Planchart","doi":"10.1007/s12640-023-00658-z","DOIUrl":"10.1007/s12640-023-00658-z","url":null,"abstract":"β-N-Methylamino-L-alanine (BMAA) is a non-proteinogenic amino acid produced by cyanobacteria, which has been implicated in several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS). It is postulated that chronic exposure to BMAA can lead to formation of protein aggregates, oxidative stress, and/or excitotoxicity, which are mechanisms involved in the etiology of ALS. While specific genetic mutations are identified in some instances of ALS, it is likely that a combination of genetic and environmental factors, such as exposure to the neurotoxin BMAA, contributes to disease. We used a transgenic zebrafish with an ALS-associated mutation, compared with wild-type fish to explore the potential neurotoxic effects of BMAA through chronic long-term exposures. While our results revealed low concentrations of BMAA in the brains of exposed fish, we found no evidence of decreased swim performance or behavioral differences that might be reflective of neurodegenerative disease. Further research is needed to determine if chronic BMAA exposure in adult zebrafish is a suitable model to study neurodegenerative disease initiation and/or progression.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 5","pages":"481-495"},"PeriodicalIF":2.9,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11216512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10231702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CNTN1 in the Nucleus Accumbens is Involved in Methamphetamine-Induced Conditioned Place Preference in Mice. 小鼠凹凸核中的 CNTN1 参与了甲基苯丙胺诱导的条件性位置偏好。

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-08-01 Epub Date: 2023-04-04 DOI: 10.1007/s12640-023-00640-9

Linxuan Zhang, Zehao Zeng, Xiaoyu Lu, Mengqing Li, Jiayu Yao, Guangjing Zou, Zhaorong Chen, Qian Li, Changqi Li, Fang Li

{"title":"CNTN1 in the Nucleus Accumbens is Involved in Methamphetamine-Induced Conditioned Place Preference in Mice.","authors":"Linxuan Zhang, Zehao Zeng, Xiaoyu Lu, Mengqing Li, Jiayu Yao, Guangjing Zou, Zhaorong Chen, Qian Li, Changqi Li, Fang Li","doi":"10.1007/s12640-023-00640-9","DOIUrl":"10.1007/s12640-023-00640-9","url":null,"abstract":"Methamphetamine (Meth), a commonly used central nervous system stimulant, is highly addictive. Currently, there is no effective treatment for Meth dependence and abuse, although cell adhesion molecules (CAMs) have been shown to play an important role in the formation and remodeling of synapses in the nervous system while also being involved in addictive behavior. Contactin 1 (CNTN1) is a CAM that is widely expressed in the brain; nevertheless, its role in Meth addiction remains unclear. Therefore, in the present study, we established mouse models of single and repeated Meth exposure and subsequently determined that CNTN1 expression in the nucleus accumbens (NAc) was upregulated in mice following single or repeated Meth exposure, whereas CNTN1 expression in the hippocampus was not significantly altered. Intraperitoneal injection of the dopamine receptor 2 antagonist haloperidol reversed Meth-induced hyperlocomotion and upregulation of CNTN1 expression in the NAc. Additionally, repeated Meth exposure also induced conditioned place preference (CPP) in mice and upregulated the expression levels of CNTN1, NR2A, NR2B, and PSD95 in the NAc. Using an AAV-shRNA-based approach to specifically silence CNTN1 expression in the NAc via brain stereotaxis reversed Meth-induced CPP and decreased the expression levels of NR2A, NR2B, and PSD95 in the NAc. These findings suggest that CNTN1 expression in the NAc plays an important role in Meth-induced addiction, and the underlying mechanism may be related to the expression of synapse-associated proteins in the NAc. The results of this study improved our understanding of the role of cell adhesion molecules in Meth addiction.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 4","pages":"324-337"},"PeriodicalIF":3.7,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9896282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Connexin 43 Promotes Neurogenesis via Regulating Aquaporin-4 after Cerebral Ischemia. 脑缺血后，Connexin 43 通过调节 Aquaporin-4 促进神经发生

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-08-01 Epub Date: 2023-04-19 DOI: 10.1007/s12640-023-00646-3

Heling Chu, Jing Dong, Yuping Tang, Chuyi Huang, Qihao Guo

{"title":"Connexin 43 Promotes Neurogenesis via Regulating Aquaporin-4 after Cerebral Ischemia.","authors":"Heling Chu, Jing Dong, Yuping Tang, Chuyi Huang, Qihao Guo","doi":"10.1007/s12640-023-00646-3","DOIUrl":"10.1007/s12640-023-00646-3","url":null,"abstract":"We aimed to test the effects of connexin43 (Cx43) on ischemic neurogenesis and examined whether it was dependent on aquaporin-4 (AQP4). We detected the expression of Cx43 and AQP4 in the ipsilateral subventricular zone (SVZ) and peri-infarct cortex after middle cerebral artery occlusion (MCAO). Also, we examined neurogenesis in the above regions via co-labeling of 5-bromo-2-deoxyuridine (BrdU)/neuronal nuclear antigen (NeuN) and BrdU/doublecortin (DCX). The effects of Cx43 and AQP4 were investigated by using two transgenic animals: heterozygous Cx43 (Cx43±) mice and AQP4 knockout (AQP4-/-) mice, and connexin mimetic peptide (CMP), a selective Cx43 blocker. We demonstrated AQP4 and Cx43 were co-expressed in the astrocytes after MCAO and the expression was highly increased in ipsilateral SVZ and peri-infarct cortex. Cx43± mice had larger infarction volumes and worse neurological function. Both BrdU/NeuN and BrdU/DCX co-labeled cells in the two regions were reduced in Cx43± and AQP4-/- mice compared to wild-type (WT) mice, suggesting Cx43 and AQP4 participated in neurogenesis of neural stem cells. Moreover, CMP decreased AQP4 expression and inhibited neurogenesis in WT mice, while the latter failed to be observed in AQP4-/- mice. Besides, higher levels of IL-1β and TNF-α were detected in the SVZ and peri-infarct cortex of AQP4-/- and Cx43± mice than those in WT mice. In conclusion, our data suggest that Cx43 elicits neuroprotective effects after cerebral ischemia through promoting neurogenesis in the SVZ to regenerate the injured neurons, which is AQP4 dependent and associated with down-regulation of inflammatory cytokines IL-1β and TNF-α.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 4","pages":"349-361"},"PeriodicalIF":3.7,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9858583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Microglial Priming in Bilirubin-Induced Neurotoxicity. 胆红素诱导的神经毒性中的小胶质细胞诱导作用

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-08-01 Epub Date: 2023-04-14 DOI: 10.1007/s12640-023-00643-6

Hongmei Huang, Siyu Li, Yan Zhang, Chunmei He, Ziyu Hua

{"title":"Microglial Priming in Bilirubin-Induced Neurotoxicity.","authors":"Hongmei Huang, Siyu Li, Yan Zhang, Chunmei He, Ziyu Hua","doi":"10.1007/s12640-023-00643-6","DOIUrl":"10.1007/s12640-023-00643-6","url":null,"abstract":"Neuroinflammation is a major contributor to bilirubin-induced neurotoxicity, which results in severe neurological deficits. Microglia are the primary immune cells in the brain, with M1 microglia promoting inflammatory injury and M2 microglia inhibiting neuroinflammation. Controlling microglial inflammation could be a promising therapeutic strategy for reducing bilirubin-induced neurotoxicity. Primary microglial cultures were prepared from 1-3-day-old rats. In the early stages of bilirubin treatment, pro-/anti-inflammatory (M1/M2) microglia mixed polarization was observed. In the late stages, bilirubin persistence induced dominant proinflammatory microglia, forming an inflammatory microenvironment and inducing iNOS expression as well as the release of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β. Simultaneously, nuclear factor-kappa B (NF-κB) was activated and translocated into the nucleus, upregulating inflammatory target genes. As well known, neuroinflammation can have an effect on N-methyl-D-aspartate receptor (NMDAR) expression or function, which is linked to cognition. Treatment with bilirubin-treated microglia-conditioned medium did affect the expression of IL-1β, NMDA receptor subunit 2A (NR2A), and NMDA receptor subunit 2B (NR2B) in neurons. However, VX-765 effectively reduces the levels of proinflammatory cytokines TNF-α, IL-6, and IL-1β, as well as the expressions of CD86, and increases the expressions of anti-inflammatory related Arg-1. A timely reduction in proinflammatory microglia could protect against bilirubin-induced neurotoxicity.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 4","pages":"338-348"},"PeriodicalIF":3.7,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9842056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to: Protective Role of Epigallocatechin Gallate in a Rat Model of Cisplatin-Induced Cerebral Inflammation and Oxidative Damage: Impact of Modulating NF-κB and Nrf2. 更正：表没食子儿茶素没食子酸酯在顺铂诱导的大鼠脑炎症和氧化损伤模型中的保护作用：调节 NF-κB 和 Nrf2 的影响。

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-08-01 DOI: 10.1007/s12640-023-00642-7

Manar Hamed Arafa, Hebatallah Husseini Atteia

引用次数: 0

Posttreatment with Ospemifene Attenuates Hypoxia- and Ischemia-Induced Apoptosis in Primary Neuronal Cells via Selective Modulation of Estrogen Receptors. 通过选择性调节雌激素受体，奥司匹芬后处理可减轻缺氧和缺血诱导的原发性神经元细胞凋亡

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-08-01 Epub Date: 2023-05-02 DOI: 10.1007/s12640-023-00644-5

Bernadeta A Pietrzak, Agnieszka Wnuk, Karolina Przepiórska, Andrzej Łach, Małgorzata Kajta

{"title":"Posttreatment with Ospemifene Attenuates Hypoxia- and Ischemia-Induced Apoptosis in Primary Neuronal Cells via Selective Modulation of Estrogen Receptors.","authors":"Bernadeta A Pietrzak, Agnieszka Wnuk, Karolina Przepiórska, Andrzej Łach, Małgorzata Kajta","doi":"10.1007/s12640-023-00644-5","DOIUrl":"10.1007/s12640-023-00644-5","url":null,"abstract":"Stroke and perinatal asphyxia have detrimental effects on neuronal cells, causing millions of deaths worldwide each year. Since currently available therapies are insufficient, there is an urgent need for novel neuroprotective strategies to address the effects of cerebrovascular accidents. One such recent approach is based on the neuroprotective properties of estrogen receptors (ERs). However, activation of ERs by estrogens may contribute to the development of endometriosis or hormone-dependent cancers. Therefore, in this study, we utilized ospemifene, a novel selective estrogen receptor modulator (SERM) already used in dyspareunia treatment. Here, we demonstrated that posttreatment with ospemifene in primary neocortical cell cultures subjected to 18 h of hypoxia and/or ischemia followed by 6 h of reoxygenation has robust neuroprotective potential. Ospemifene partially reverses hypoxia- and ischemia-induced changes in LDH release, the degree of neurodegeneration, and metabolic activity. The mechanism of the neuroprotective actions of ospemifene involves the inhibition of apoptosis since the compound decreases caspase-3 overactivity during hypoxia and enhances mitochondrial membrane potential during ischemia. Moreover, in both models, ospemifene decreased the levels of the proapoptotic proteins BAX, FAS, FASL, and GSK3β while increasing the level of the antiapoptotic protein BCL2. Silencing of specific ERs showed that the neuroprotective actions of ospemifene are mediated mainly via ESR1 (during hypoxia and ischemia) and GPER1 (during hypoxia), which is supported by ospemifene-evoked increases in ESR1 protein levels in hypoxic and ischemic neurons. The results identify ospemifene as a promising neuroprotectant, which in the future may be used to treat injuries due to brain hypoxia/ischemia.","PeriodicalId":19193,"journal":{"name":"Neurotoxicity Research","volume":"41 4","pages":"362-379"},"PeriodicalIF":3.7,"publicationDate":"2023-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10354152/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9844695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to: Baicalin Attenuates Ketamine-Induced Neurotoxicity in the Developing Rats: Involvement of PI3K/Akt and CREB/BDNF/Bcl-2 Pathways. 更正：黄芩苷可减轻氯胺酮诱导的发育期大鼠神经毒性：PI3K/Akt和CREB/BDNF/Bcl-2途径的参与。

IF 3.7 3区医学

Neurotoxicity Research Pub Date : 2023-08-01 DOI: 10.1007/s12640-023-00641-8

Daiying Zuo, Li Lin, Yumiao Liu, Chengna Wang, Jingwen Xu, Feng Sun, Lin Li, Zengqiang Li, Yingliang Wu

引用次数: 0