Chinese Journal of Physiology最新文献_第7页

GATA-binding protein 4 promotes neuroinflammation and cognitive impairment in Aβ_1-42 fibril-infused rats through small nucleolar RNA host gene 1/miR-361-3p axis. gata结合蛋白4通过小核仁RNA宿主基因1/miR-361-3p轴促进Aβ1-42原纤维灌注大鼠的神经炎症和认知功能障碍。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2023-01-01 DOI: 10.4103/cjop.CJOP-D-22-00057

Lidan Liu, Yanhui Peng, Wenping Liu, Jiajun Xu, Dali Li, Xiuwen Li

{"title":"GATA-binding protein 4 promotes neuroinflammation and cognitive impairment in Aβ1-42 fibril-infused rats through small nucleolar RNA host gene 1/miR-361-3p axis.","authors":"Lidan Liu, Yanhui Peng, Wenping Liu, Jiajun Xu, Dali Li, Xiuwen Li","doi":"10.4103/cjop.CJOP-D-22-00057","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-22-00057","url":null,"abstract":"Aging with dysregulated metabolic and immune homeostasis stimulates pyroptosis, neuroinflammation, and cellular senescence, thus contributing to etiopathogenesis of Alzheimer's disease. GATA-binding protein 4 (GATA4) functions as a transcriptional factor in response to DNA damage, and is associated with neuroinflammation and cellular senescence. The role of GATA4 in Alzheimer's disease was investigated. GATA4 was elevated in hippocampus of Aβ1-42 fibril-infused rats. Injection with shRNA targeting GATA4 reduced escape latency with increase of time in target quadrant and number of platform crossings in Aβ1-42 fibril-infused rats. Moreover, knockdown of GATA4 ameliorated morphological changes of hippocampus and reduced amyloid plaque deposition in Aβ1-42 fibril-infused rats. Silence of GATA4 repressed neuroinflammation and apoptosis in Aβ1-42 fibril-infused rats. Loss of GATA4 in Aβ1-42 fibril-infused rats reduced the expression of specificity protein 1 (Sp1) to downregulate long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) and upregulated miR-361-3p. Loss of SNHG1 ameliorated learning and memory impairments in Aβ1-42 fibril-infused rats. Overexpression of Sp1 attenuated GATA4 silence-induced decrease of escape latency, increase of time in target quadrant, and number of platform crossings in Aβ1-42 fibril-infused rats. In conclusion, silence of GATA4 ameliorated cognitive dysfunction and inhibited hippocampal inflammation and cell apoptosis through regulation of Sp1/SNHG1/miR-361-3p.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10772540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Cholinergic deficiency in the cholinergic system as a pathogenetic link in the formation of various syndromes in COVID-19. 胆碱能系统胆碱能缺乏是COVID-19各种综合征形成的一个发病环节。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2023-01-01 DOI: 10.4103/cjop.CJOP-D-22-00072

Sergey Petrovich Lysenkov, Dmitriy Vitalevich Muzhenya, Aminat Ramazanovna Tuguz, Tamara Ur'evna Urakova, Dmitriy Sergeevich Shumilov, Ibragim Askarbievich Thakushinov, Rustem Askarbievich Thakushinov, Elena Anatolevna Tatarkova, Diana Muratovna Urakova

{"title":"Cholinergic deficiency in the cholinergic system as a pathogenetic link in the formation of various syndromes in COVID-19.","authors":"Sergey Petrovich Lysenkov, Dmitriy Vitalevich Muzhenya, Aminat Ramazanovna Tuguz, Tamara Ur'evna Urakova, Dmitriy Sergeevich Shumilov, Ibragim Askarbievich Thakushinov, Rustem Askarbievich Thakushinov, Elena Anatolevna Tatarkova, Diana Muratovna Urakova","doi":"10.4103/cjop.CJOP-D-22-00072","DOIUrl":"https://doi.org/10.4103/cjop.CJOP-D-22-00072","url":null,"abstract":"According to recent data, several mechanisms of viral invasion of the central nervous system (CNS) have been proposed, one of which is both direct penetration of the virus through afferent nerve fibers and damage to the endothelium of cerebral vessels. It has been proven that the SARS-CoV-2 virus affects pathologically not only the human cardiorespiratory system but is also associated with a wide range of neurological diseases, cerebrovascular accidents, and neuromuscular pathologies. However, the observed post-COVID symptom complex in patients, manifested in the form of headache, \"fog in the head,\" high temperature, muscle weakness, lowering blood pressure, does it make us think about the pathophysiological mechanisms that contribute to the development of this clinical picture? One possible explanation is a disruption in the signaling of the acetylcholine system (AChS) in the body. Viral invasions, and in particular COVID-19, can negatively affect the work of the AChS, disrupting its coordination activities. Therefore, the main goal of this literature review is to analyze the information and substantiate the possible mechanisms for the occurrence of post-COVID syndrome in people who have had COVID-19 from the standpoint of AChS dysfunctions.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10754146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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: 1

Beta-hydroxy-beta-methylbutyrate supplementation preserves fat-free mass in collegiate boxers during acute body mass loss β -羟基- β -甲基丁酸盐补充保留无脂肪质量在急性体重损失的大学拳击手

4区医学

Chinese Journal of Physiology Pub Date : 2023-01-01 DOI: 10.4103/cjop.cjop-d-23-00074

Chen-Kang Chang, Shih-Yen Kao, Chung-Yuan Wang

引用次数: 0

LncRNA colorectal neoplasia differentially expressed promotes glycolysis of liver cancer cells by regulating hypoxia-inducible factor 1α. LncRNA结直肠癌差异表达通过调控缺氧诱导因子1α促进肝癌细胞糖酵解。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365458

Dan Tang, Lijin Zhao, Rui Mu, Yu Ao, Xuyang Zhang, Xiongxiong Li

{"title":"LncRNA colorectal neoplasia differentially expressed promotes glycolysis of liver cancer cells by regulating hypoxia-inducible factor 1α.","authors":"Dan Tang, Lijin Zhao, Rui Mu, Yu Ao, Xuyang Zhang, Xiongxiong Li","doi":"10.4103/0304-4920.365458","DOIUrl":"https://doi.org/10.4103/0304-4920.365458","url":null,"abstract":"LncRNAs are associated with tumorigenesis of liver cancer. LncRNA Colorectal Neoplasia Differentially Expressed (CRNDE) was identified as an oncogenic lncRNA and involved in tumor growth and metastasis. The role of CRNDE in liver cancer was investigated. CRNDE was elevated in liver cancer cells. Knockdown of CRNDE decreased cell viability and inhibited proliferation of liver cancer. Moreover, knockdown of CRNDE reduced levels of extracellular acidification rate, glucose consumption, and lactate production to repress glycolysis of liver cancer. Silence of CRNDE enhanced the expression of miR-142 and reduced enhancer of zeste homolog 2 (EZH2) and hypoxia-inducible factor 1α (HIF-1α). Over-expression of HIF-1α attenuated CRNDE silence-induced decrease of glucose consumption and lactate production. Injection with sh-CRNDE virus reduced in vivo tumor growth of liver cancer through up-regulation of miR-142 and down-regulation of EZH2 and HIF-1α. In conclusion, knockdown of CRNDE suppressed cell proliferation, glycolysis, and tumor growth of liver cancer through EZH2/miR-142/HIF-1α.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10522919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

The role of exercise intensity on fatty liver in rats. 运动强度对大鼠脂肪肝的影响。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365461

Xueyan Gu, Xiaocui Ma, Limin Mo, Qiyu Wang

{"title":"The role of exercise intensity on fatty liver in rats.","authors":"Xueyan Gu, Xiaocui Ma, Limin Mo, Qiyu Wang","doi":"10.4103/0304-4920.365461","DOIUrl":"https://doi.org/10.4103/0304-4920.365461","url":null,"abstract":"Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is often caused by obesity. Currently, moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) are two effective treatments for reducing fat mass in patients with obesity and NAFLD. However, the comparative fat-reducing effects and underlying molecular mechanisms of MICT and HIIT remain unclear. This comprehensive study was performed on male Wistar rats treated with standard diet, high-fat diet, MICT, and HIIT to explore their comparative fat-reducing effects and corresponding molecular mechanisms. HIIT had a greater effect on hepatic vacuolation density and lipid content reduction than MICT, and triglyceride and total cholesterol levels in the serum and the liver demonstrated different sensitivities to different exercise training programs. At the molecular level, both MICT and HIIT altered the processes of fatty acid synthesis, fatty acid transport, fatty acid β-oxidation, and cholesterol synthesis, wherein the transcriptional and translational levels of signaling molecules peroxisome proliferator-activated receptors (PPARs) regulating fatty acid and cholesterol synthesis were strongly changed. Moreover, the metabolic pathways of amino acids, bile acids, and carbohydrates were also affected according to transcriptome analysis, and the changes in the above-mentioned processes in the HIIT group were greater than those in the MICT group. In combination with the search tool for the retrieval of interacting genes/proteins (STRING) analysis and the role of PPARs in lipid metabolism, as well as the expression pattern of PPARs in the MICT and HIIT groups, the MICT-and HIIT-induced fat loss was mediated by the PPAR pathway, causing feedback responses in fatty acid, steroid, amino acid, bile acid, and carbohydrate metabolism, and HIIT had a better fat-reducing effect, which may be initiated by PPAR-α. This study provides a theoretical basis for targeted therapy of patients with obesity and NAFLD.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10466566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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: 1

Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats. 优化运动预处理时间对大鼠运动性心力损伤的保护作用。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365457

Zheng Ping, Jinyu Li, Yawei Sun, Xiaoli Zhang, Ziwen Wang, Xuebin Cao

{"title":"Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats.","authors":"Zheng Ping, Jinyu Li, Yawei Sun, Xiaoli Zhang, Ziwen Wang, Xuebin Cao","doi":"10.4103/0304-4920.365457","DOIUrl":"https://doi.org/10.4103/0304-4920.365457","url":null,"abstract":"The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10466567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Overexpression of long non-coding RNA LINC00158 inhibits neuronal apoptosis by promoting autophagy in spinal cord injury. 长链非编码RNA LINC00158过表达通过促进脊髓损伤自噬抑制神经元凋亡。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.360035

Fuchuang Qin, Guorong He, Yu Sun, Guangning Chen, Qijian Yu, Xilie Ma

{"title":"Overexpression of long non-coding RNA LINC00158 inhibits neuronal apoptosis by promoting autophagy in spinal cord injury.","authors":"Fuchuang Qin, Guorong He, Yu Sun, Guangning Chen, Qijian Yu, Xilie Ma","doi":"10.4103/0304-4920.360035","DOIUrl":"https://doi.org/10.4103/0304-4920.360035","url":null,"abstract":"Spinal cord injury (SCI) is a common central nervous system disease. It is reported that long non-coding RNA LINC00158 is involved in the process of SCI. The purpose of this study was to explore the biological role of LINC00158 in the SCI. First, we established a rat SCI model by surgical method and evaluated the motor function of rats by the Basso-Beattie-Bresnahan locomotor rating scale. The results showed that the expression of LINC00158 decreased and apoptotic cells increased in the SCI model rats. Meanwhile, we found the upregulated LC3-II/LC3-I, Beclin-1, and p62 in the SCI rats. Then, primary rat spinal cord neurons were exposed to oxygen/glucose deprivation (OGD) as an in vitro cell model of SCI. After OGD treatment, the expression of LINC00158 decreased significantly and the apoptosis of spinal cord neurons increased. OGD treatment resulted in upregulation of LC3-II/LC3-I and Beclin-1 and downregulation of p62 in primary spinal cord neurons, which could be eliminated by overexpression of LINC00158. 3-Methyladenine and chloroquine (autophagy inhibitor) reversed the inhibitory effect of LINC00158 overexpression on apoptosis of primary spinal cord neurons. In conclusion, this study demonstrated that LINC00158 overexpression repressed neuronal apoptosis by promoting autophagy, suggesting that LINC00158 may be a potential therapeutic target in the SCI.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10522917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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: 1

Sensitivity of Ca²⁺-sensing receptor-transient receptor potential-mediated Ca²⁺ influx to extracellular acidity in bEND.3 endothelial cells. Ca2+感应受体-瞬时受体电位介导的Ca2+内流对弯曲细胞外酸度的敏感性。3个内皮细胞。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365460

Iat-Lon Leong, Chung-Ming Yu, Lian-Ru Shiao, Paul Chan, King-Chuen Wu, Yuk-Man Leung

{"title":"Sensitivity of Ca2+-sensing receptor-transient receptor potential-mediated Ca2+ influx to extracellular acidity in bEND.3 endothelial cells.","authors":"Iat-Lon Leong, Chung-Ming Yu, Lian-Ru Shiao, Paul Chan, King-Chuen Wu, Yuk-Man Leung","doi":"10.4103/0304-4920.365460","DOIUrl":"https://doi.org/10.4103/0304-4920.365460","url":null,"abstract":"Ca2+-sensing receptors (CaSRs) are G protein-coupled receptors activated by elevated concentrations of extracellular Ca2+. In our previous works, we showed protein and functional expression of CaSR in mouse cerebral endothelial cell (EC) (bEND.3); the CaSR response (high Ca2+-elicited cytosolic [Ca2+] elevation) was unaffected by suppression of phospholipase C but in part involved Ca2+ influx through transient receptor potential V1 (TRPV1) channels. In this work, we investigated if extracellular acidity affected CaSR-mediated Ca2+ influx triggered by high (3 mM) Ca2+ (CaSR agonist), 3 mM spermine (CaSR agonist), and 10 mM cinacalcet (positive allosteric modulator of CaSR). Extracellular acidosis (pH 6.8 and pH 6.0) strongly suppressed cytosolic [Ca2+] elevation triggered by high Ca2+, spermine, and cinacalcet; acidosis also inhibited Mn2+ influx stimulated by high Ca2+ and cinacalcet. Purinoceptor-triggered Ca2+ response, however, was not suppressed by acidosis. Extracellular acidity also did not affect membrane potential, suggesting suppressed CaSR-mediated Ca2+ influx in acidity did not result from the reduced electrical driving force for Ca2+. Our results suggest Ca2+ influx through a putative CaSR-TRP complex in bEND.3 EC was sensitive to extracellular pH.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10522918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Leonurine suppresses prostate cancer growth in vitro and in vivo by regulating miR-18a-5p/SLC40A1 axis. 益母鼠尿通过调控miR-18a-5p/SLC40A1轴抑制前列腺癌体外和体内生长。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-11-01 DOI: 10.4103/0304-4920.365459

Bin Liang, Shouxi Cui, Songnian Zou

引用次数: 2

Study on the role of naringin in attenuating Trimethylamine-N-Oxide-Induced human umbilical vein endothelial cell inflammation, oxidative stress, and endothelial dysfunction. 柚皮苷对三甲胺- n -氧化物诱导的人脐静脉内皮细胞炎症、氧化应激和内皮功能障碍作用的研究。

IF 1.8 4区医学

Chinese Journal of Physiology Pub Date : 2022-09-01 DOI: 10.4103/0304-4920.359796

Hui Zhao, Jianping Zhao

{"title":"Study on the role of naringin in attenuating Trimethylamine-N-Oxide-Induced human umbilical vein endothelial cell inflammation, oxidative stress, and endothelial dysfunction.","authors":"Hui Zhao, Jianping Zhao","doi":"10.4103/0304-4920.359796","DOIUrl":"https://doi.org/10.4103/0304-4920.359796","url":null,"abstract":"Trimethylamine-N-oxide (TMAO), a phospholipid metabolite, can modulate cholesterol synthesis and promote vascular inflammation and endothelial dysfunction, thereby increasing the risk of atherosclerosis (AS). Previously, it was found that naringin reduced damage to human umbilical vein endothelial cells (HUVECs) triggered by oxidized low-density lipoprotein. This article continues to explore the role and mechanism of naringin in protecting HUVECs from TMAO-induced damage. After the construction of TMAO-induced AS model in HUVECs, inflammation, oxidative stress, and endothelial function were examined by real-time quantitative polymerase chain reaction, Western blotting, nitric oxide (NO), reactive oxygen species (ROS), superoxide dismutase, and malondialdehyde (MDA) kits. Results showed that naringin pretreatment inhibited endothelial inflammation and oxidative stress, promoted NO release, and inhibited the degradation of Zona occludens-2, occludin, and vascular endothelial-cadherin, thereby restoring the functional and structural integrity of the endothelium. Furthermore, the addition of mitogen-activated protein kinase (MAPK) agonist demonstrated that the therapeutic effect of naringin was achieved through inactivating TMAO-stimulated MAPK signaling in HUVECs.","PeriodicalId":10251,"journal":{"name":"Chinese Journal of Physiology","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2022-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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: 1