The Kaohsiung journal of medical sciences最新文献

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Emergence of clonal evolution with Philadelphia chromosome in acute myeloid leukemia after hypomethylation agents and BCL2 inhibitor treatment. 低甲基化药物和 BCL2 抑制剂治疗后,急性髓性白血病出现费城染色体克隆进化。
The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-08-19 DOI: 10.1002/kjm2.12886
Shih-Yu Kao, Samuel Y Hsiao, Bi-Hua Du, Hui-Hua Hsiao
{"title":"Emergence of clonal evolution with Philadelphia chromosome in acute myeloid leukemia after hypomethylation agents and BCL2 inhibitor treatment.","authors":"Shih-Yu Kao, Samuel Y Hsiao, Bi-Hua Du, Hui-Hua Hsiao","doi":"10.1002/kjm2.12886","DOIUrl":"10.1002/kjm2.12886","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"947-948"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142001670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
CMTM5 influences Hippo/YAP axis to promote ferroptosis in glioma through regulating WWP2-mediated LATS2 ubiquitination. CMTM5通过调节WWP2介导的LATS2泛素化影响Hippo/YAP轴,促进胶质瘤中的铁变态反应。
The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-08-21 DOI: 10.1002/kjm2.12889
Ye Fan, He-Qin Zou
{"title":"CMTM5 influences Hippo/YAP axis to promote ferroptosis in glioma through regulating WWP2-mediated LATS2 ubiquitination.","authors":"Ye Fan, He-Qin Zou","doi":"10.1002/kjm2.12889","DOIUrl":"10.1002/kjm2.12889","url":null,"abstract":"<p><p>Glioma, a common malignancy, is characterized by high morbidity and mortality. Promoting ferroptosis can delay tumor progression. Here, we aimed to explore the underlying mechanism of ferroptosis in glioma. In vitro and in vivo experiments were conducted using glioma cells and nude mice. The expression of genes and proteins was evaluated by RT-qPCR, Western blot assay, and immunohistochemical staining. Malignant activities of glioma cells were evaluated using MTT, EdU, and Transwell assays. The levels of Fe<sup>2+</sup>, lipid reactive oxygen species, and malondialdehyde were determined using commercial kits. The interplays among CMTM5, WWP2, and LATS2 were validated using Co-immunoprecipitation assay. The UALCAN database predicted downregulation of CMTM5 expression in glioma, and low expression of CMTM5 was associated with poor survival outcomes. CMTM5 overexpression inhibited cell growth and invasion and promoted ferroptosis of glioma cells. Besides, CMTM5 protein interacted with WWP2 protein and decreased WWP2 expression. WWP2 silencing attenuated LATS2 ubiquitination to enhance LATS2 expression and phosphorylation of YAP1. CMTM5 exerted a suppressive effect on cell growth and invasion and promoted ferroptosis of glioma cells by regulating the WWP2/LATS2 pathway. In the in vivo experiments, CMTM5 overexpression suppressed tumor growth and enhanced ferroptosis. CMTM5 regulated Hippo/YAP signaling to inhibit cell growth and invasion and to promote ferroptosis in glioma by regulating WWP2-mediated LATS2 ubiquitination, thereby attenuating glioma progression.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"890-902"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142020053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction: 'ASPM predicts poor prognosis and regulates cell proliferation in bladder cancer'. Zhen-Ya Gao, Fang Yu, Huan-Xia Jia, Zhuo Ye, Shi-Jie Yao, Kaohsiung J Med Sci. 2020; 36: 1021-1029 (https://doi.org/10.1002/kjm2.12284). 撤稿:《ASPM预测膀胱癌不良预后并调控细胞增殖》。Zhen-Ya Gao, Fang Yu, Huan-Xia Jia, Zhuo Ye, Shi-Jie Yao, Kaohsiung J Med Sci. 2020; 36: 1021-1029 (https://doi.org/10.1002/kjm2.12284).
The Kaohsiung journal of medical sciences Pub Date : 2024-10-01 Epub Date: 2024-03-28 DOI: 10.1002/kjm2.12825
{"title":"Retraction: 'ASPM predicts poor prognosis and regulates cell proliferation in bladder cancer'. Zhen-Ya Gao, Fang Yu, Huan-Xia Jia, Zhuo Ye, Shi-Jie Yao, Kaohsiung J Med Sci. 2020; 36: 1021-1029 (https://doi.org/10.1002/kjm2.12284).","authors":"","doi":"10.1002/kjm2.12825","DOIUrl":"10.1002/kjm2.12825","url":null,"abstract":"<p><p>The above article, published online on 06 August 2020, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor-in-Chief, Wan-Long Chuang, and John Wiley and Sons Australia, Ltd. The retraction has been agreed due to a high degree of similarity and duplication of figures previously published in five identified articles. The authors are unable to determine how the images published were copies of figures from other articles. Following the investigation by the Editors, the conclusions of this article are considered unreliable due to the high degree of duplication and the questionable origin of the data.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"955"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140308446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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 “miR‐199a/214 cluster enhances prostate cancer sensitiveness to nimotuzumab via targeting TBL1XR1” 对 "miR-199a/214基因簇通过靶向TBL1XR1增强前列腺癌对尼莫妥珠单抗的敏感性 "的更正
The Kaohsiung journal of medical sciences Pub Date : 2024-09-19 DOI: 10.1002/kjm2.12897
{"title":"Correction to “miR‐199a/214 cluster enhances prostate cancer sensitiveness to nimotuzumab via targeting TBL1XR1”","authors":"","doi":"10.1002/kjm2.12897","DOIUrl":"https://doi.org/10.1002/kjm2.12897","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Molecular mechanism of ALKBH5‐mediated m6A demethylation regulating lipopolysaccharide‐induced epithelial–mesenchymal transition in sepsis‐induced acute kidney injury ALKBH5 介导的 m6A 去甲基化调控脂多糖诱导的脓毒症急性肾损伤上皮-间质转化的分子机制
The Kaohsiung journal of medical sciences Pub Date : 2024-09-17 DOI: 10.1002/kjm2.12892
Hai‐Hong Zhao, Chun‐Ling Chen, Fen‐Fang Chen, Lu‐Lu Zhang, Mei‐Mei Li, Ze‐Bao He
{"title":"Molecular mechanism of ALKBH5‐mediated m6A demethylation regulating lipopolysaccharide‐induced epithelial–mesenchymal transition in sepsis‐induced acute kidney injury","authors":"Hai‐Hong Zhao, Chun‐Ling Chen, Fen‐Fang Chen, Lu‐Lu Zhang, Mei‐Mei Li, Ze‐Bao He","doi":"10.1002/kjm2.12892","DOIUrl":"https://doi.org/10.1002/kjm2.12892","url":null,"abstract":"This study explored the mechanism by which the m6A demethylase ALKBH5 mediates epithelial–mesenchymal transition (EMT) in sepsis‐associated acute kidney injury (SA‐AKI) and AKI‐chronic kidney disease (CKD) transition. HK‐2 cells were stimulated with lipopolysaccharide (LPS) to establish an in vitro model of SA‐AKI. ALKBH5 expression was reduced through the transfection of si‐ALKBH5. Cell viability, apoptosis, and migration were detected by CCK‐8 assay, TUNEL staining, and Transwell. The levels of TNF‐α, IL‐1β, and IL‐6 were measured by enzyme‐linked immunosorbent assay. Quantitative real‐time polymerase chain reaction or Western blotting was performed to determine the expressions of ALKBH5, miR‐205‐5p, DDX5, E‐cadherin, and α‐SMA. The m6A level was quantitatively analyzed. The expression of pri‐miR‐205 bound to DGCR8 and m6A‐modified pri‐miR‐205 after intervention with ALKBH5 expression was detected by RNA immunoprecipitation. A dual‐luciferase assay confirmed the binding between miR‐205‐5p and DDX5. ALKBH5 was highly expressed in LPS‐induced HK‐2 cells. Inhibition of ALKBH5 increased cell viability, repressed apoptosis, and reduced EMT. Inhibition of ALKBH5 increased the m6A modification level, thereby promoting DGCR8 binding to pri‐miR‐205 to increase miR‐205‐5p expression and eventually targeting DDX5 expression. Low expression of miR‐205‐5p or overexpression of DDX5 partially abolished the inhibitory effect of ALKBH5 silencing on EMT. In conclusion, ALKBH5 represses miR‐205‐5p expression by removing m6A modification to upregulate DDX5 expression, thereby promoting EMT and AKI‐CKD transition after SA‐AKI.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142257965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MicroRNA‐223 alleviates inflammatory response in renal ischemia‐reperfusion injury by targeting NLRP3 MicroRNA-223 通过靶向 NLRP3 减轻肾缺血再灌注损伤的炎症反应
The Kaohsiung journal of medical sciences Pub Date : 2024-09-06 DOI: 10.1002/kjm2.12883
Jun Ye, Xiaoli Tang, Ming Li, Yutian Liao, Yiqian Zeng, Furong Tang, Eryue Qiu
{"title":"MicroRNA‐223 alleviates inflammatory response in renal ischemia‐reperfusion injury by targeting NLRP3","authors":"Jun Ye, Xiaoli Tang, Ming Li, Yutian Liao, Yiqian Zeng, Furong Tang, Eryue Qiu","doi":"10.1002/kjm2.12883","DOIUrl":"https://doi.org/10.1002/kjm2.12883","url":null,"abstract":"We investigated the potential correlation between miR‐223 and NAcHT, LRR, and PYd domain‐containing protein 3 (NLRP3) in the context of renal ischemia‐reperfusion injury (RIRI), which is a leading cause of acute renal failure with significant mortality rates. Additionally, miR‐223 has been implicated in renal inflammation, further highlighting its relevance to this study. C57BL/6 male mice were used as RIRI models. After successful modeling, pathological examinations and serum creatinine and miR‐223 levels were tested. Pro‐inflammatory cytokine (IL‐1β, IL‐6, IL‐8, NLPR3, TLR4) expression was detected in mice by western blot (kidney tissue) and enzyme‐linked immunosorbent assay (serum). HK‐2 cells were used for in vitro experiments. A hypoxia/reoxygenation (H/R) model was used, and miR‐223 and pro‐inflammatory cytokine levels were detected using PCR and western blot assays, respectively. A dual‐luciferase reporter assay was conducted to confirm the binding of miR‐223 to NLPR3. Next, NLRP3 was knocked down to determine whether the anti‐inflammatory function of miR‐223 is dependent on NLRP3. MiR‐223 expression was lower in RIRI mice than in the sham operation group. The level of miR‐223 negatively correlated with serum creatinine levels and the severity of tubule injury. Increased proinflammatory cytokine levels in RIRI mice were observed. In vitro, miR‐223 alleviated the inflammatory response in H/R treated cells by inhibiting proinflammatory cytokines. Dual‐luciferase reporter and western blot assays confirmed the binding of miR‐223 to NLRP3. NLRP3 knockdown reversed the anti‐inflammatory effects of miR‐223 in HK‐2 cells. MiR‐223 plays an anti‐inflammatory role in RIRI by targeting NLRP3 to repress pro‐inflammatory factors.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142202809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Self-knotted feeding jejunostomy tube in an esophageal cancer patient: A case report and review of the literature. 食管癌患者的自结进食空肠造口管:病例报告和文献综述。
The Kaohsiung journal of medical sciences Pub Date : 2024-09-01 Epub Date: 2024-06-11 DOI: 10.1002/kjm2.12869
Po-Hsuan Wu, Pei-Shan Weng
{"title":"Self-knotted feeding jejunostomy tube in an esophageal cancer patient: A case report and review of the literature.","authors":"Po-Hsuan Wu, Pei-Shan Weng","doi":"10.1002/kjm2.12869","DOIUrl":"10.1002/kjm2.12869","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"865-866"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141302357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Liquid silicone gel injection leading to primary squamous cell carcinoma of the breast. 液体硅凝胶注射导致乳腺原发性鳞状细胞癌。
The Kaohsiung journal of medical sciences Pub Date : 2024-09-01 Epub Date: 2024-07-29 DOI: 10.1002/kjm2.12874
Hidenobu Takahashi, Yen-Shuo Huang, Chee-Yin Chai, Jung-Yu Kan
{"title":"Liquid silicone gel injection leading to primary squamous cell carcinoma of the breast.","authors":"Hidenobu Takahashi, Yen-Shuo Huang, Chee-Yin Chai, Jung-Yu Kan","doi":"10.1002/kjm2.12874","DOIUrl":"10.1002/kjm2.12874","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"862-864"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141790703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Enhancing therapeutic potential: Human adipose-derived mesenchymal stem cells modified with recombinant adeno-associated virus expressing VEGF165 gene for peripheral nerve injury. 增强治疗潜力:用表达 VEGF165 基因的重组腺相关病毒修饰的人脂肪间充质干细胞治疗周围神经损伤。
The Kaohsiung journal of medical sciences Pub Date : 2024-09-01 Epub Date: 2024-08-05 DOI: 10.1002/kjm2.12875
Shuai Jiang, Bo Chen, Zhen-Yu Sun
{"title":"Enhancing therapeutic potential: Human adipose-derived mesenchymal stem cells modified with recombinant adeno-associated virus expressing VEGF165 gene for peripheral nerve injury.","authors":"Shuai Jiang, Bo Chen, Zhen-Yu Sun","doi":"10.1002/kjm2.12875","DOIUrl":"10.1002/kjm2.12875","url":null,"abstract":"<p><p>This study aimed to investigate the therapeutic potential of human adipose-derived mesenchymal stem cells (hADSCs) modified with recombinant adeno-associated virus (rAAV) carrying the vascular endothelial growth factor 165 (VEGF165) gene in peripheral nerve injury (PNI). The hADSCs were categorized into blank, control (transduced with rAAV control vector), and VEGF165 (transduced with rAAV VEGF165 vector) groups. Subsequently, Schwann cell differentiation was induced, and Schwann cell markers were assessed. The sciatic nerve injury mouse model received injections of phosphate-buffered saline (PBS group), PBS containing hADSCs (hADSCs group), rAAV control vector (control-hADSCs group), or rAAV VEGF165 vector (VEGF165-hADSCs group) into the nerve defect site. Motor function recovery, evaluated through the sciatic function index (SFI), and nerve regeneration, assessed via toluidine blue staining along with scrutiny of Schwann cell markers and neurotrophic factors, were conducted. Modified hADSCs exhibited enhanced Schwann cell differentiation and elevated expression of Schwann cell markers [S100 calcium-binding protein B (S100B), NGF receptor (NGFR), and glial fibrillary acidic protein (GFAP)]. Mice in the VEGF165-hADSCs group demonstrated improved motor function recovery compared to those in the other three groups, accompanied by increased fiber diameter, axon diameter, and myelin thickness, as well as elevated expression of Schwann cell markers (S100B, NGFR, and GFAP) and neurotrophic factors [mature brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF)] in the distal nerve segment. rAAV-VEGF165 modification enhances hADSC potential in PNI, promoting motor recovery and nerve regeneration. Elevated Schwann cell markers and neurotrophic factors underscore therapy benefits, providing insights for nerve injury strategies.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"819-829"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Exploring the diagnostic potential of immunoglobulin A-microbiota interplay in liver cirrhosis and spontaneous bacterial peritonitis. 探索肝硬化和自发性细菌性腹膜炎中免疫球蛋白 A-微生物群相互作用的诊断潜力。
The Kaohsiung journal of medical sciences Pub Date : 2024-09-01 Epub Date: 2024-07-18 DOI: 10.1002/kjm2.12876
Liang-Jie Zhang, Wen-Qi Huang, Yuan Zhang, You-Lian Zhou, Hao-Ming Xu, Chong Zhao, Yu-Qiang Nie
{"title":"Exploring the diagnostic potential of immunoglobulin A-microbiota interplay in liver cirrhosis and spontaneous bacterial peritonitis.","authors":"Liang-Jie Zhang, Wen-Qi Huang, Yuan Zhang, You-Lian Zhou, Hao-Ming Xu, Chong Zhao, Yu-Qiang Nie","doi":"10.1002/kjm2.12876","DOIUrl":"10.1002/kjm2.12876","url":null,"abstract":"<p><p>The human gut microbiota significantly impacts health, including liver conditions like liver cirrhosis (LC) and spontaneous bacterial peritonitis (SBP). Immunoglobulin A (IgA) plays a central role in maintaining gut microbial balance. Understanding IgA's interplay with gut microbiota and liver health is crucial. This study explores the relationship between fecal IgA levels, gut microbiota, and liver injury severity. A total of 69 LC patients and 30 healthy controls were studied. Fecal IgA levels were measured using ELISA, and IgA-coated bacteria were quantified via flow cytometry. Microbiota diversity and composition were assessed through 16S rRNA sequencing. Liver injury severity was graded using the Child-Pugh score. Statistical analyses determined correlations. LC patients had higher fecal IgA levels than controls, correlating positively with liver injury severity. Microbiota diversity decreased with severity, accompanied by shifts in composition favoring pro-inflammatory species. Ralstonia abundance positively correlated with liver injury, whereas Faecalibacterium showed a negative correlation. Specific microbial markers for SBP were identified. Functional profiling revealed altered microbial functionalities in LC and SBP. Elevated fecal IgA levels, coupled with microbiota alterations, correlate with liver injury severity in LC patients. Modulating gut microbiota could be a promising strategy for managing liver-related conditions. Further research is needed to understand underlying mechanisms and translate findings into clinical practice, potentially improving patient outcomes.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"837-851"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141636333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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