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Synaptotagmin 13 Could Drive the Progression of Esophageal Squamous Cell Carcinoma Through Upregulating ACRV1. 突触表蛋白 13 可通过上调 ACRV1 推动食管鳞状细胞癌的进展
DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-07-24 DOI: 10.1089/dna.2024.0106
Longlong Shao, Bin Li
{"title":"Synaptotagmin 13 Could Drive the Progression of Esophageal Squamous Cell Carcinoma Through Upregulating ACRV1.","authors":"Longlong Shao, Bin Li","doi":"10.1089/dna.2024.0106","DOIUrl":"10.1089/dna.2024.0106","url":null,"abstract":"<p><p>SYT13 is one of the atypical members of the synaptotagmin (SYT) family whose function has attracted considerable attention in recent years. Although SYT13 has been studied in several types of human cancers, such as lung cancer, its role in esophageal squamous cell carcinoma (ESCC) is still unclear. It was demonstrated that SYT13 is significantly upregulated in ESCC tissues compared with normal ones and correlated with higher degree of malignancy. Knockdown of SYT13 could inhibit ESCC cell proliferation and migration, while promoting cell apoptosis. Meanwhile, ESCC cells with relatively lower SYT13 expression grew slower <i>in vivo</i> and finally formed smaller xenografts. Furthermore, acrosomal vesicular protein 1 was identified as a potential downstream target of SYT13, which regulates cell phenotypes of ESCC cells in cooperation with SYT13. All the <i>in vitro</i> and <i>in vivo</i> results in this study identified that SYT13 silencing could be an effective strategy to inhibit the development of ESCC, which could be considered as a promising therapeutic target in the treatment of ESCC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"452-462"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141763438","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
Bone Marrow Mesenchymal Stem Cells-Derived Extracellular Vesicle miR-208a-3p Alleviating Spinal Cord Injury via Regulating the Biological Function of Spinal Cord Neurons. 骨髓间充质干细胞衍生的细胞外囊泡 miR-208a-3p 通过调节脊髓神经元的生物功能缓解脊髓损伤
DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-08-12 DOI: 10.1089/dna.2024.0064
Jianwei Yang, Yanhua Yao
{"title":"Bone Marrow Mesenchymal Stem Cells-Derived Extracellular Vesicle miR-208a-3p Alleviating Spinal Cord Injury via Regulating the Biological Function of Spinal Cord Neurons.","authors":"Jianwei Yang, Yanhua Yao","doi":"10.1089/dna.2024.0064","DOIUrl":"10.1089/dna.2024.0064","url":null,"abstract":"<p><p>We aim to explore the potential mechanism of bone marrow mesenchymal stem cells-derived extracellular vesicles (BMSCs-Exo) in improving spinal cord injury (SCI). Thirty male 12-week specific pathogen-free (SPF) Sprague-Dawley (SD) rats were used to construct SCI model <i>in vivo</i>. Ten male 12-week SPF SD rats were used to extract BMSCs. The Basso, Beattie, Bresnahan (BBB) score was used to evaluate the motor function of rats. Real-time fluorescence quantitative PCR (RT-PCR), western blot (WB), and double luciferase assay were used to explore the regulation between rno-miR-208a-3p and Cdkn1a (p21) in BMSCs. Primary spinal cord neurons were treated with lipopolysaccharide (100 ng/mL) for 30 min to mimic SCI <i>in vitro</i>. Compared with the model group (14 scores), BMSCs-Exo increased BBB score (19 scores) in SCI rats. Compared with the sham group, Cdkn1a was upregulated, whereas rno-miR-208a-3p was downregulated in the model group. However, compared with the model group, Cdkn1a was downregulated, whereas rno-miR-208a-3p was upregulated in the BMSCs-Exo group. In addition, rno-miR-208a-3p inhibited the expression of Cdkn1a via direct binding way. BMSCs-Exo-rno-miR-208a-3p promoted the proliferation of primary spinal neurons via inhibiting apoptosis <i>in vitro</i>. Moreover, BMSCs-Exo-rno-miR-208a-3p promoted cyclin D1, CDK6, and Bcl-2 and inhibited Bax expression in a cell model of SCI. In conclusion, BMSCs-Exo-carried rno-miR-208a-3p significantly protects rats from SCI via regulating the Cdkn1a pathway.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"463-473"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141918388","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
The Role of Neddylation in Malaria Parasites. Neddylation在疟疾寄生虫中的作用
DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-06-17 DOI: 10.1089/dna.2024.0120
Plabita Paul, Bandita Nayak, Satish Mishra
{"title":"The Role of Neddylation in Malaria Parasites.","authors":"Plabita Paul, Bandita Nayak, Satish Mishra","doi":"10.1089/dna.2024.0120","DOIUrl":"10.1089/dna.2024.0120","url":null,"abstract":"<p><p><i>Plasmodium</i> parasites, the causative agents of malaria, rely on sophisticated cellular mechanisms to survive and proliferate within their hosts. <i>Plasmodium</i> complex life cycle requires posttranslational modifications (PTMs) to control cellular activities. Neddylation is a type of PTM in which NEDD8 is covalently attached to target proteins and plays an important role in cell cycle control and metabolism. Covalent attachment to its substrates requires the Nedd8-activating enzyme, E1; the NEDD8-conjugating enzyme, E2; and the ligase, E3. In <i>Plasmodium</i>, protein neddylation is essential for parasite development during the stage I-II transition from zygote to ookinete differentiation and malaria transmission. Here, we discuss the current understanding of protein neddylation in <i>Plasmodium,</i> which is involved in malaria transmission.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"426-429"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141422227","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
Polo-Like Kinase 1 and DNA Damage Response. Polo-Like Kinase 1 与 DNA 损伤反应
DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-07-03 DOI: 10.1089/dna.2024.0018
Wei Li, Yongjian Hao
{"title":"Polo-Like Kinase 1 and DNA Damage Response.","authors":"Wei Li, Yongjian Hao","doi":"10.1089/dna.2024.0018","DOIUrl":"10.1089/dna.2024.0018","url":null,"abstract":"<p><p>Polo-like kinase 1 (Plk1), an evolutionarily conserved serine/threonine protein kinase, is a key regulator involved in the mitotic process of the cell cycle. Mounting evidence suggests that Plk1 is also involved in a variety of nonmitotic events, including the DNA damage response, DNA replication, cytokinesis, embryonic development, apoptosis, and immune regulation. The DNA damage response (DDR) includes activation of the DNA checkpoint, DNA damage recovery, DNA repair, and apoptosis. Plk1 is not only an important target of the G2/M DNA damage checkpoint but also negatively regulates the G2/M checkpoint commander Ataxia telangiectasia-mutated (ATM), promotes G2/M phase checkpoint recovery, and regulates homologous recombination repair by interacting with Rad51 and BRCA1, the key factors of homologous recombination repair. This article briefly reviews the function of Plk1 in response to DNA damage.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"430-437"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141499949","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
Innovating Cancer Treatment Through Cell Cycle, Telomerase, Angiogenesis, and Metastasis. 通过细胞周期、端粒酶、血管生成和转移创新癌症治疗。
DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-07-17 DOI: 10.1089/dna.2024.0109
Tooba Yousefi, Bahareh Mohammadi Jobani, Reyhaneh Taebi, Durdi Qujeq
{"title":"Innovating Cancer Treatment Through Cell Cycle, Telomerase, Angiogenesis, and Metastasis.","authors":"Tooba Yousefi, Bahareh Mohammadi Jobani, Reyhaneh Taebi, Durdi Qujeq","doi":"10.1089/dna.2024.0109","DOIUrl":"10.1089/dna.2024.0109","url":null,"abstract":"<p><p>Cancer remains a formidable challenge in the field of medicine, necessitating innovative therapeutic strategies to combat its relentless progression. The cell cycle, a tightly regulated process governing cell growth and division, plays a pivotal role in cancer development. Dysregulation of the cell cycle allows cancer cells to proliferate uncontrollably. Therapeutic interventions designed to disrupt the cell cycle offer promise in restraining tumor growth and progression. Telomerase, an enzyme responsible for maintaining telomere length, is often overactive in cancer cells, conferring them with immortality. Targeting telomerase presents an opportunity to limit the replicative potential of cancer cells and hinder tumor growth. Angiogenesis, the formation of new blood vessels, is essential for tumor growth and metastasis. Strategies aimed at inhibiting angiogenesis seek to deprive tumors of their vital blood supply, thereby impeding their progression. Metastasis, the spread of cancer cells from the primary tumor to distant sites, is a major challenge in cancer therapy. Research efforts are focused on understanding the underlying mechanisms of metastasis and developing interventions to disrupt this deadly process. This review provides a glimpse into the multifaceted approach to cancer therapy, addressing critical aspects of cancer biology-cell cycle regulation, telomerase activity, angiogenesis, and metastasis. Through ongoing research and innovative strategies, the field of oncology continues to advance, offering new hope for improved treatment outcomes and enhanced quality of life for cancer patients.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"438-451"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141636236","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
Rosalind Franklin Society Proudly Announces the 2023 Award Recipient for DNA and Cell Biology. 罗莎琳德-富兰克林学会自豪地宣布 2023 年 DNA 和细胞生物学奖得主。
DNA and cell biology Pub Date : 2024-09-01 DOI: 10.1089/dna.2024.22445.rfs2023
Wanda Marini
{"title":"Rosalind Franklin Society Proudly Announces the 2023 Award Recipient for <i>DNA and Cell Biology</i>.","authors":"Wanda Marini","doi":"10.1089/dna.2024.22445.rfs2023","DOIUrl":"https://doi.org/10.1089/dna.2024.22445.rfs2023","url":null,"abstract":"","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":"43 9","pages":"425"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142304563","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
Histidine Kinase QseC in Glaesserella parasuis Enhances the Secretion of Proinflammatory Cytokines by Macrophages via the p38 and NF-κB Signaling Pathways. 寄生褐藻中的组氨酸激酶 QseC 通过 p38 和 NF-κB 信号通路促进巨噬细胞分泌促炎细胞因子。
DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-07-24 DOI: 10.1089/dna.2024.0078
Xuefeng Yan, Congwei Gu, Zehui Yu, Mingde Zhao, Lvqin He
{"title":"Histidine Kinase QseC in <i>Glaesserella parasuis</i> Enhances the Secretion of Proinflammatory Cytokines by Macrophages via the p38 and NF-κB Signaling Pathways.","authors":"Xuefeng Yan, Congwei Gu, Zehui Yu, Mingde Zhao, Lvqin He","doi":"10.1089/dna.2024.0078","DOIUrl":"10.1089/dna.2024.0078","url":null,"abstract":"<p><p>The <i>qseC</i> gene is a two-component system that encodes a histidine protein kinase and is highly conserved among different <i>Glaesserella parasuis</i> strains. In this study, we used qRT-PCR and enzyme-linked immunosorbent assay to confirm that Toll-like receptor 4 (TLR4) plays a role in the expression of proinflammatory cytokines interleukin (IL)-1β and IL-6 by stimulating RAW 264.7 macrophages with QseC. Furthermore, we revealed that blocking the p38 and NF-κB pathways that regulate signaling can significantly reduce the production of proinflammatory cytokines induced by QseC. In summary, our data suggest that QseC is a novel proinflammatory mediator that induces TLR4-dependent proinflammatory activity in RAW 264.7 macrophages through the p38 and NF-κB pathways.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"474-481"},"PeriodicalIF":0.0,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141763437","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
ANGPTL4 Stabilizes Bone Morphogenetic Protein 7 Through Deubiquitination and Promotes HCC Proliferation via the SMAD/MAPK Pathway. ANGPTL4 通过去泛素化稳定骨形态发生蛋白 7 并通过 SMAD/MAPK 途径促进 HCC 增殖
DNA and cell biology Pub Date : 2024-08-01 Epub Date: 2024-06-03 DOI: 10.1089/dna.2024.0022
Yun Bai, Guanghua Cui, Xiaoke Sun, Meiqi Wei, Yanying Liu, Jialu Guo, Yu Yang
{"title":"ANGPTL4 Stabilizes Bone Morphogenetic Protein 7 Through Deubiquitination and Promotes HCC Proliferation via the SMAD/MAPK Pathway.","authors":"Yun Bai, Guanghua Cui, Xiaoke Sun, Meiqi Wei, Yanying Liu, Jialu Guo, Yu Yang","doi":"10.1089/dna.2024.0022","DOIUrl":"10.1089/dna.2024.0022","url":null,"abstract":"<p><p>This study aimed to determine the function of angiopoietin-related protein 4 (ANGPTL4) and bone morphogenetic protein 7 (BMP7) on hepatocellular carcinoma (HCC). Overexpressing plasmids were cotransfected into HepG2 cells to determine the interaction between ANGPTL4 and BMP7. The effect of ANGPTL4 on the stability of BMP7 is examined by detecting the expression and ubiquitination levels. <i>In vitro</i> and <i>in vivo</i> experiments of knocking down ANGPTL4 while overexpressing BMP7 were performed to investigate whether the effects of ANGPTL4 on HCC proliferation, migration, and downstream signaling pathways were dependent on BMP7. ANGPTL4 is able to interact with BMP7, and knockdown of ANGPTL4 increased BMP7 expression and ubiquitination. Overexpression of BMP7 reversed the inhibition of HCC proliferation and migration as well as the decrease in the expression levels of Smad1/5/8 and MAPK14 caused by knockdown of ANGPTL4. ANGPTL4 promotes the proliferation and migration of HCC by inhibiting the ubiquitination degradation of BMP7 and the Smad/MAPK pathway, providing a novel mechanism and a potential therapeutic target for the treatment of HCC.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"395-400"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141201538","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
Low and High-Normal FMR1 Triplet Cytosine, Guanine Guanine Repeats Affect Ovarian Reserve and Fertility in Women Who Underwent In Vitro Fertilization Treatment? Results from a Cross-Sectional Study. FMR1三重胞嘧啶、鸟嘌呤重复序列的低正常值和高正常值会影响接受体外受精治疗的妇女的卵巢储备功能和生育能力吗？一项横断面研究的结果。
DNA and cell biology Pub Date : 2024-08-01 Epub Date: 2024-06-18 DOI: 10.1089/dna.2023.0395
Ana Carolina Vasconcelos Nunes, Camila Martins Trevisan, Carla Peluso, Flavia Althman Loureiro, Alexandre Torchio Dias, Daniel Rincon, Fernando Luiz Affonso Fonseca, Denise Maria Christofolini, Antonio Simone Laganà, Erik Montagna, Caio Parente Barbosa, Bianca Bianco
{"title":"Low and High-Normal <i>FMR1</i> Triplet Cytosine, Guanine Guanine Repeats Affect Ovarian Reserve and Fertility in Women Who Underwent <i>In Vitro</i> Fertilization Treatment? Results from a Cross-Sectional Study.","authors":"Ana Carolina Vasconcelos Nunes, Camila Martins Trevisan, Carla Peluso, Flavia Althman Loureiro, Alexandre Torchio Dias, Daniel Rincon, Fernando Luiz Affonso Fonseca, Denise Maria Christofolini, Antonio Simone Laganà, Erik Montagna, Caio Parente Barbosa, Bianca Bianco","doi":"10.1089/dna.2023.0395","DOIUrl":"10.1089/dna.2023.0395","url":null,"abstract":"<p><p>Dynamic mutations in the 5' untranslated region of <i>FMR1</i> are associated with infertility. Premutation alleles interfere with prenatal development and increase infertility risks. The number of CGG repeats that causes the highest decrease in ovarian reserves remains unclear. We evaluated the effect of <i>FMR1</i> CGG repeat lengths on ovarian reserves and <i>in vitro</i> fertilization (IVF) treatment outcomes in 272 women with alleles within the normal range. <i>FMR1</i> CGG repeat length was investigated via PCR and capillary electrophoresis. Alleles were classified as low-normal, normal, and high-normal. Serum levels of follicle-stimulating hormone and anti-Mullerian hormone (AMH) in the follicular phase of the menstrual cycle were measured, and antral follicles (AFC) were counted. IVF outcomes were collected from medical records. Regarding <i>FMR1</i> CGG repeat length alleles, 63.2% of women presented at least one low-normal allele. Those carrying low-normal alleles had significantly lower AMH levels than women carrying normal or high-normal alleles. Low-normal/low-normal genotype was the most frequent, followed by low-normal/normal and normal/normal. A comparison of ovarian reserve markers and reproductive outcomes of the three most frequent genotypes revealed that AFC in the low-normal/normal genotype was significantly lower than the low-normal/low-normal genotype. The low number of <i>FMR1</i> CGG repeats affected AMH levels and AFC but not IVF outcomes per cycle of treatment.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"414-424"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141422226","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
RNA Isoforms as Broad Targets for Cancer Immunotherapy. 作为癌症免疫疗法广泛靶点的 RNA 异构体。
DNA and cell biology Pub Date : 2024-08-01 Epub Date: 2024-05-21 DOI: 10.1089/dna.2024.0108
Guangyuan Li, Nathan Salomonis
{"title":"RNA Isoforms as Broad Targets for Cancer Immunotherapy.","authors":"Guangyuan Li, Nathan Salomonis","doi":"10.1089/dna.2024.0108","DOIUrl":"10.1089/dna.2024.0108","url":null,"abstract":"<p><p>While immunotherapy is typically reserved for cancer patients with a high mutational burden, neoantigens produced from post-transcriptional regulation provide a possible untapped reservoir of common immunogenic targets for new targeted cancer therapies. In this review, we describe new and emerging technologies, unconventional molecular targets and challenges for the precision immune targeting of diverse malignancies. In particular, we focus on the unique potential of targeting alternative mRNA isoforms as a source for broadly presented neoantigens and cell surface proteins. Finally, we discuss emerging challenges for alternative isoform immune targeting, with an emphasis <i>in silico</i> prioritization and high-throughput target validation.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"363-368"},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141072432","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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