PPAR Research最新文献_第10页

Treatment of Diabetic Mice with a Combination of Ketogenic Diet and Aerobic Exercise via Modulations of PPARs Gene Programs. 通过调节PPARs基因程序，结合生酮饮食和有氧运动治疗糖尿病小鼠。

IF 2.9 3区医学

PPAR Research Pub Date : 2018-03-20 eCollection Date: 2018-01-01 DOI: 10.1155/2018/4827643

Qiang Zhang, Lingyan Xu, Jie Xia, Dongmei Wang, Min Qian, Shuzhe Ding

{"title":"Treatment of Diabetic Mice with a Combination of Ketogenic Diet and Aerobic Exercise via Modulations of PPARs Gene Programs.","authors":"Qiang Zhang, Lingyan Xu, Jie Xia, Dongmei Wang, Min Qian, Shuzhe Ding","doi":"10.1155/2018/4827643","DOIUrl":"10.1155/2018/4827643","url":null,"abstract":"Type 2 diabetes is a prevalent chronic disease arising as a serious public health problem worldwide. Diet intervention is considered to be a critical strategy in glycemic control of diabetic patients. Recently, the low-carbohydrate ketogenic diet is shown to be effective in glycemic control and weight loss. However, hepatic lipid accumulation could be observed in mice treated with ketogenic diet. On the other hand, exercise is a well-known approach for treating nonalcoholic fatty liver disease. We thus hypothesize that the combination of ketogenic diet and exercise could improve insulin sensitivity, while minimizing adverse effect of hepatic steatosis. In order to test this hypothesis, we established diabetic mice model with streptozotocin (STZ) and divided them into control group, ketogenic diet group, and ketogenic diet with aerobic exercise group. We found that after six weeks of intervention, mice treated with ketogenic diet and ketogenic diet combined with exercise both have lower body weights, HbAlc level, HOMA index, and improvements in insulin sensitivity, compared with diabetes group. In addition, mice in ketogenic diet intervention exhibited hepatic steatosis shown by serum and hepatic parameters, as well as histochemistry staining in the liver, which could be largely relieved by exercise. Furthermore, gene analysis revealed that ketogenic diet in combination with exercise reduced PPARγ and lipid synthetic genes, as well as enhancing PPARα and lipid β-oxidation gene program in the liver compared to those in ketogenic diet without exercise. Overall, the present study demonstrated that the combination of ketogenic diet and a moderate-intensity aerobic exercise intervention improved insulin sensitivity in diabetic mice, while avoiding hepatic steatosis, which provided a novel strategy in the combat of diabetes.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"4827643"},"PeriodicalIF":2.9,"publicationDate":"2018-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/4827643","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36083798","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: 27

High Glucose Induces Autophagy through PPARγ-Dependent Pathway in Human Nucleus Pulposus Cells. 高糖通过ppar γ依赖途径诱导人髓核细胞自噬。

IF 2.9 3区医学

PPAR Research Pub Date : 2018-03-01 eCollection Date: 2018-01-01 DOI: 10.1155/2018/8512745

Chang Jiang, Shuhao Liu, Yuanwu Cao, Hongping Shan

{"title":"High Glucose Induces Autophagy through PPARγ-Dependent Pathway in Human Nucleus Pulposus Cells.","authors":"Chang Jiang, Shuhao Liu, Yuanwu Cao, Hongping Shan","doi":"10.1155/2018/8512745","DOIUrl":"https://doi.org/10.1155/2018/8512745","url":null,"abstract":"Diabetes mellitus is a multiorgan disorder affecting many types of connective tissues, including bone and cartilage. High glucose could accelerate the autophagy in nucleus pulposus (NP) cells. In our present study, we investigated whether peroxisome proliferator-activated receptor γ (PPAR-γ) pathway is involved into autophagy regulation in NP cells under high glucose condition. After NP cells were treated with different high glucose concentrations for 72 hours, the rate of autophagy increased. Moreover, the levels of PPARγ, Beclin-1, and LC3II were significantly increased and p62 was significantly decreased compared to control group. Then, NP cells were treated with high glucose plus PPARγ agonist or PPARγ antagonist, respectively. The rate of autophagy and the levels of Beclin-1 and LC3II increased, but p62 decreased when PPARγ agonist was used. On the contrary, the rate of autophagy and the levels of Beclin-1 and LC3II decreased, while p62 increased when PPARγ antagonist was added. These results suggested that autophagy induced by high glucose in NP cells was through PPARγ-dependent pathway.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"8512745"},"PeriodicalIF":2.9,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/8512745","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36036571","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: 8

PPARγ Antagonizes Hypoxia-Induced Activation of Hepatic Stellate Cell through Cross Mediating PI3K/AKT and cGMP/PKG Signaling. PPARγ通过交叉介导PI3K/AKT和cGMP/PKG信号通路拮抗缺氧诱导的肝星状细胞活化。

IF 2.9 3区医学

PPAR Research Pub Date : 2018-03-01 eCollection Date: 2018-01-01 DOI: 10.1155/2018/6970407

Qinghui Zhang, Shihao Xiang, Qingqian Liu, Tao Gu, Yongliang Yao, Xiaojie Lu

{"title":"PPARγ Antagonizes Hypoxia-Induced Activation of Hepatic Stellate Cell through Cross Mediating PI3K/AKT and cGMP/PKG Signaling.","authors":"Qinghui Zhang, Shihao Xiang, Qingqian Liu, Tao Gu, Yongliang Yao, Xiaojie Lu","doi":"10.1155/2018/6970407","DOIUrl":"https://doi.org/10.1155/2018/6970407","url":null,"abstract":"Background and aims: Accumulating evidence reveals that PPARγ plays a unique role in the regulation of hepatic fibrosis and hepatic stellate cells (HSCs) activation. This study was aimed at investigating the role of PPARγ in hypoxia-induced hepatic fibrogenesis and its possible mechanism.Methods: Rats used for CCl4-induced hepatic fibrosis model were exposed to hypoxia for 8 hours each day. Rats exposed to hypoxia were treated with or without the PPARγ agonist rosiglitazone. Liver sections were stained with HE and Sirius red staining 8 weeks later. HSCs were exposed to hypoxic environment in the presence or absence of rosiglitazone, and expression of PPARγ and two fibrosis markers, α-SMA and desmin, were measured using western blot and immunofluorescence staining. Next, levels of PPARγ, α-SMA, and desmin as well as PKG and cGMP activity were detected using PI3K/AKT and a cGMP activator or inhibitor.Results: Hypoxia promoted the induction and progress of hepatic fibrosis and HSCs activation. Meanwhile, rosiglitazone significantly antagonized the effects induced by hypoxia. Signaling by sGC/cGMP/PKG promoted the inhibitory effect of PPARγ on hypoxia-induced activation of HSCs. Moreover, PI3K/AKT signaling or PDE5 blocked the above response of PPARγ.Conclusion: sGC/cGMP/PKG and PI3K/AKT signals act on PPARγ synergistically to attenuate hypoxia-induced HSC activation.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"6970407"},"PeriodicalIF":2.9,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/6970407","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36036570","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: 20

Research Advances in the Correlation between Peroxisome Proliferator-Activated Receptor-γ and Digestive Cancers. 过氧化物酶体增殖物激活受体-γ与消化道肿瘤相关性研究进展。

IF 2.9 3区医学

PPAR Research Pub Date : 2018-02-01 eCollection Date: 2018-01-01 DOI: 10.1155/2018/5289859

Shuqi Xu, Xuanfu Xu

引用次数: 7

Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ. 马齿苋提取物通过激活PPARγ减轻硫酸葡聚糖钠诱导小鼠结肠炎的发展。

IF 2.9 3区医学

PPAR Research Pub Date : 2018-02-01 eCollection Date: 2018-01-01 DOI: 10.1155/2018/6079101

Rui Kong, Hui Luo, Nan Wang, Jingjing Li, Shizan Xu, Kan Chen, Jiao Feng, Liwei Wu, Sainan Li, Tong Liu, Xiya Lu, Yujing Xia, Yanhong Shi, Yingqun Zhou, Weigang He, Qi Dai, Yuejuan Zheng, Jie Lu

{"title":"Portulaca Extract Attenuates Development of Dextran Sulfate Sodium Induced Colitis in Mice through Activation of PPARγ.","authors":"Rui Kong, Hui Luo, Nan Wang, Jingjing Li, Shizan Xu, Kan Chen, Jiao Feng, Liwei Wu, Sainan Li, Tong Liu, Xiya Lu, Yujing Xia, Yanhong Shi, Yingqun Zhou, Weigang He, Qi Dai, Yuejuan Zheng, Jie Lu","doi":"10.1155/2018/6079101","DOIUrl":"https://doi.org/10.1155/2018/6079101","url":null,"abstract":"Portulaca oleracea L. is a traditional Chinese medicine, which has been used as adjuvant therapy for inflammatory bowel disease (IBD). However, the mechanism of its activity in IBD still remains unclear. Since previous studies have documented the anti-inflammatory effect of peroxisome proliferator activated receptors-γ (PPAR-γ), Portulaca regulation of PPAR-γ in inflammation was examined in current study. Ulcerative colitis (UC) was generated by 5% dextran sulfate sodium (DSS) in mice and four groups were established as normal control, DSS alone, DSS plus mesalamine, and DSS plus Portulaca. Severity of UC was evaluated by body weight, stool blood form, and length of colorectum. Inflammation was examined by determination of inflammatory cytokines (TNF-a, IL-6, and IL-1a). Portulaca extract was able to attenuate development of UC in DSS model similar to the treatment of mesalazine. Moreover, Portulaca extract inhibited proinflammatory cytokines release and reduced the level of DSS-induced NF-κB phosphorylation. Furthermore, Portulaca extract restored PPAR-γ level, which was reduced by DSS. In addition, Portulaca extract protected DSS induced apoptosis in mice. In conclusion, Portulaca extract can alleviate colitis in mice through regulation of inflammatory reaction, apoptosis, and PPAR-γ level; therefore, Portulaca extract can be a potential candidate for the treatment of IBD.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"6079101"},"PeriodicalIF":2.9,"publicationDate":"2018-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/6079101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35864432","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: 26

Peroxisome Proliferator-Activated Receptor γ and PGC-1α in Cancer: Dual Actions as Tumor Promoter and Suppressor. 过氧化物酶体增殖物激活受体γ和PGC-1α在癌症中的双重作用:肿瘤启动子和抑制子。

IF 2.9 3区医学

PPAR Research Pub Date : 2018-01-21 eCollection Date: 2018-01-01 DOI: 10.1155/2018/6727421

Seong-Hoon Yun, Sang-Heum Han, Joo-In Park

{"title":"Peroxisome Proliferator-Activated Receptor γ and PGC-1α in Cancer: Dual Actions as Tumor Promoter and Suppressor.","authors":"Seong-Hoon Yun, Sang-Heum Han, Joo-In Park","doi":"10.1155/2018/6727421","DOIUrl":"https://doi.org/10.1155/2018/6727421","url":null,"abstract":"Peroxisome proliferator-activated receptor γ (PPARγ) is part of a nuclear receptor superfamily that regulates gene expression involved in cell differentiation, proliferation, immune/inflammation response, and lipid metabolism. PPARγ coactivator-1α (PGC-1α), initially identified as a PPARγ-interacting protein, is an important regulator of diverse metabolic pathways, such as oxidative metabolism and energy homeostasis. The role of PGC-1α in diabetes, neurodegeneration, and cardiovascular disease is particularly well known. PGC-1α is also now known to play important roles in cancer, independent of the role of PPARγ in cancer. Though many researchers have studied the expression and clinical implications of PPARγ and PGC-1α in cancer, there are still many controversies about the role of PPARγ and PGC-1α in cancer. This review examines and summarizes some recent data on the role and action mechanisms of PPARγ and PGC-1α in cancer, respectively, particularly the recent progress in understanding the role of PPARγ in several cancers since our review was published in 2012.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"6727421"},"PeriodicalIF":2.9,"publicationDate":"2018-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2018/6727421","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35961728","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: 41

Vascular Remodeling, Oxidative Stress, and Disrupted PPARγ Expression in Rats of Long-Term Hyperhomocysteinemia with Metabolic Disturbance. 长期高同型半胱氨酸血症伴代谢紊乱大鼠的血管重塑、氧化应激和 PPARγ 表达紊乱

IF 3.5 3区医学

PPAR Research Pub Date : 2018-01-15 eCollection Date: 2018-01-01 DOI: 10.1155/2018/6738703

Yajing Huo, Xuqing Wu, Jing Ding, Yang Geng, Weiwei Qiao, Anyan Ge, Cen Guo, Jianing Lv, Haifeng Bao, Wei Fan

{"title":"Vascular Remodeling, Oxidative Stress, and Disrupted PPARγ Expression in Rats of Long-Term Hyperhomocysteinemia with Metabolic Disturbance.","authors":"Yajing Huo, Xuqing Wu, Jing Ding, Yang Geng, Weiwei Qiao, Anyan Ge, Cen Guo, Jianing Lv, Haifeng Bao, Wei Fan","doi":"10.1155/2018/6738703","DOIUrl":"10.1155/2018/6738703","url":null,"abstract":"Hyperhomocysteinemia, a risk factor for vascular disease, is associated with metabolic syndrome. Our study was aimed at exploring the effect of long-term hyperhomocysteinemia with metabolic disturbances on vascular remodeling. We also studied oxidative stress and expression of PPARγ in the coronary arteriole as a possible mechanism underlying vascular remodeling. Rats were treated with standard rodent chow (Control) or diet enriched in methionine (Met) for 48 weeks. Plasma homocysteine, blood glucose, serum lipids, malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) levels were measured. Coronary arteriolar and carotid arterial remodeling was assessed by histomorphometric techniques and the expression of PPARγ in vessel wall was investigated. In Met group, an increase in the level of fasting blood glucose, serum triglyceride, total cholesterol, MDA, and NO, a decline in the serum SOD level, and increased collagen deposition in coronary and carotid arteries were found. Moreover, we detected decreased expression of PPARγ in the coronary arterioles in Met group. In summary, our study revealed metabolic disturbances in this model of long-term hyperhomocysteinemia together with vascular remodeling and suggested that impaired oxidative stress, endothelium dysfunction, and decreased PPARγ expression in the vessel wall could be underlying mechanisms.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2018 ","pages":"6738703"},"PeriodicalIF":3.5,"publicationDate":"2018-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35924883","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

Quercetin and Quercetin-Rich Red Onion Extract Alter Pgc-1α Promoter Methylation and Splice Variant Expression 槲皮素和富含槲皮素的红洋葱提取物改变Pgc-1α启动子甲基化和剪接变异表达

IF 2.9 3区医学

PPAR Research Pub Date : 2017-01-16 DOI: 10.1155/2017/3235693

Prasad P. Devarshi, Aarin D Jones, E. Taylor, B. Stefańska, T. Henagan

{"title":"Quercetin and Quercetin-Rich Red Onion Extract Alter Pgc-1α Promoter Methylation and Splice Variant Expression","authors":"Prasad P. Devarshi, Aarin D Jones, E. Taylor, B. Stefańska, T. Henagan","doi":"10.1155/2017/3235693","DOIUrl":"https://doi.org/10.1155/2017/3235693","url":null,"abstract":"Pgc-1α and its various isoforms may play a role in determining skeletal muscle mitochondrial adaptations in response to diet. 8 wks of dietary supplementation with the flavonoid quercetin (Q) or red onion extract (ROE) in a high fat diet (HFD) ameliorates HFD-induced obesity and insulin resistance in C57BL/J mice while upregulating Pgc-1α and increasing skeletal muscle mitochondrial number and function. Here, mice were fed a low fat (LF), high fat (HF), high fat plus quercetin (HF + Q), or high fat plus red onion extract (HF + RO) diet for 9 wks and skeletal muscle Pgc-1α isoform expression and DNA methylation were determined. Quantification of various Pgc-1α isoforms, including isoforms Pgc-1α-a, Pgc-1α-b, Pgc-1α-c, Pgc-1α4, total NT-Pgc-1α, and FL-Pgc-1α, showed that only total NT-Pgc-1α expression was increased in LF, HF + Q, and HF + RO compared to HF. Furthermore, Q supplementation decreased Pgc-1α-a expression compared to LF and HF, and ROE decreased Pgc-1α-a expression compared to LF. FL-Pgc-1α was decreased in HF + Q and HF + RO compared to LF and HF. HF exhibited hypermethylation at the −260 nucleotide (nt) in the Pgc-1α promoter. Q and ROE prevented HFD-induced hypermethylation. −260 nt methylation levels were associated with NT-Pgc-1α expression only. Pgc-1α isoform expression may be epigenetically regulated by Q and ROE through DNA methylation.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":" ","pages":""},"PeriodicalIF":2.9,"publicationDate":"2017-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/3235693","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48293405","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: 18

MicroRNAs-Dependent Regulation of PPARs in Metabolic Diseases and Cancers 代谢疾病和癌症中PPARs的microrna依赖性调控

IF 2.9 3区医学

PPAR Research Pub Date : 2017-01-12 DOI: 10.1155/2017/7058424

Dorothea Portius, Cyril Sobolewski, Michelangelo Foti

引用次数: 56

Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis 贝扎菲特减轻压力超载引起的心脏肥大和纤维化

IF 2.9 3区医学

PPAR Research Pub Date : 2017-01-03 DOI: 10.1155/2017/5789714

Si-Chi Xu, Zhen-Guo Ma, Wen-ying Wei, Yu-Pei Yuan, Q. Tang

{"title":"Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis","authors":"Si-Chi Xu, Zhen-Guo Ma, Wen-ying Wei, Yu-Pei Yuan, Q. Tang","doi":"10.1155/2017/5789714","DOIUrl":"https://doi.org/10.1155/2017/5789714","url":null,"abstract":"Background. Peroxisome proliferator-activated receptor-α (PPAR-α) is closely associated with the development of cardiac hypertrophy. Previous studies have indicated that bezafibrate (BZA), a PPAR-α agonist, could attenuate insulin resistance and obesity. This study was designed to determine whether BZA could protect against pressure overload-induced cardiac hypertrophy. Methods. Mice were orally given BZA (100 mg/kg) for 7 weeks beginning 1 week after aortic banding (AB) surgery. Cardiac hypertrophy was assessed based on echocardiographic, histological, and molecular aspects. Moreover, neonatal rat ventricular cardiomyocytes (NRVMs) were used to investigate the effects of BZA on the cardiomyocyte hypertrophic response in vitro. Results. Our study demonstrated that BZA could alleviate cardiac hypertrophy and fibrosis in mice subjected to AB surgery. BZA treatment also reduced the phosphorylation of protein kinase B (AKT)/glycogen synthase kinase-3β (GSK3β) and mitogen-activated protein kinases (MAPKs). BZA suppressed phenylephrine- (PE-) induced hypertrophy of cardiomyocyte in vitro. The protective effects of BZA were abolished by the treatment of the PPAR-α antagonist in vitro. Conclusions. BZA could attenuate pressure overload-induced cardiac hypertrophy and fibrosis.","PeriodicalId":20439,"journal":{"name":"PPAR Research","volume":"2017 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2017-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2017/5789714","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64688948","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: 19