Critical Reviews in Eukaryotic Gene Expression最新文献_第3页

PRMT6 promotes the immune evasion of gastric cancer via upregulating ANXA1 PRMT6 通过上调 ANXA1 促进胃癌的免疫逃避

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-03-01 DOI: 10.1615/critreveukaryotgeneexpr.2024052979

Liang Xu, Fenger Zhang, Binqi Yu, Shengnan Jia, Sunfu Fan

{"title":"PRMT6 promotes the immune evasion of gastric cancer via upregulating ANXA1","authors":"Liang Xu, Fenger Zhang, Binqi Yu, Shengnan Jia, Sunfu Fan","doi":"10.1615/critreveukaryotgeneexpr.2024052979","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024052979","url":null,"abstract":"Gastric cancer is a most malignancy in digestive tract worldwide. This study aimed to investigate the roles of PRMT6 in gastric cancer. Immunohistochemistry was performed to detect PRMT6 expression in gastric tumors. RT-qPCR was used to detected mRNA levels. Protein expression was determined using western blot. Gastric cancer cells were co-cultured with CD8+ T cells. Colony formation assay was performed to detect cell proliferation. Flow cytometry was performed to determine CD8+ T cell function and tumor cell apoptosis. PRMT6 was overexpressed in gastric tumors. High level of PRMT6 predicted poor outcomes of gastric cancer patients and inhibition of CD8+ T cell infiltration. PRMT6 promoted proliferation of CD8+ T cells and enhanced its tumor killing ability. Moreover, PRMT6 upregulated ANXA1 and promoted ANXA1 protein stability. ANXA1 overexpression suppressed the proliferation of CD8+ T cells and promoted tumor cell survival. PRMT6 functions as an oncogene in gastric cancer. PRMT6-mediated protein stability inhibits the infiltration of CD8+ T cells, resulting in immune evasion of gastric cancer. The PRMT6-ANXA1 may be a promising strategy for gastric cancer.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140316195","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

SLC7A2-mediated lysine catabolism inhibits immunosuppression in triple negative breast cancer SLC7A2- 介导的赖氨酸分解抑制了三阴性乳腺癌的免疫抑制作用

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-02-01 DOI: 10.1615/critreveukaryotgeneexpr.2024052503

Yuanyuan Sun, Yaqing Li, Chengying Jiang, Chenying Liu, Yuanming Song

{"title":"SLC7A2-mediated lysine catabolism inhibits immunosuppression in triple negative breast cancer","authors":"Yuanyuan Sun, Yaqing Li, Chengying Jiang, Chenying Liu, Yuanming Song","doi":"10.1615/critreveukaryotgeneexpr.2024052503","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024052503","url":null,"abstract":"Breast cancer is one of the most common malignancy worldwide. SLC7A2 is abnormally expressed in multi-type cancers. However, the potentials of SLC7A2 in tripe negative breast cancer (TNBC) are still unclear. This study aimed to investigate the roles of SLC7A2 and the underlying molecular mechanisms. mRNA expression was detected by RT-qPCR. The release of cytokines was detected using ELISA. Protein expression was detected by western blot. Histone crotonylation was performed using in vitro histone crotonylation assay. functional analysis was performed using CCCK-8 and flow cytometry assay. Xenografting assay was conducted to further verify the roles of SLC7A2 in TNBC. The expression of CD8A was detected using immunohistochemistry. SLC7A2 was downregulated in TNBC tumors. Low levels of SLC7A2 were associated with advanced stages and lymph node metastasis. SLC7A2 expression was positive correlated with CD8A. SLC7A2-mediated lysine catabolism drove the activation of CD8+ T cells. Moreover, SLC7A2 promoted the histone crotonylationvia upregulating ACOX1 and downregulated CDYL. SLC7A2 promoted the interaction between ACOX1 and TCF1, resulting the proliferation of CD8+ T cells. Additionally, overexpression of SLC7A2 activated CD8+ T cells and enhanced the chemosensitivity of anti-PD-1 therapies in vivo. SLC7A2 may function as an anti-tumor gene in TNBC via activating anti-tumor immunity. Therefore, SLC7A2/ ACOX1/TCF1 signaling may be promising strategy for TNBC.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139764339","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

RBM15-mediated N6-methyl adenosine (m6A) modification of EZH2 drives the epithelial-mesenchymal transition of cervical cancer RBM15介导的EZH2的N6-甲基腺苷（m6A）修饰驱动宫颈癌的上皮-间质转化

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-02-01 DOI: 10.1615/critreveukaryotgeneexpr.2024052205

Ruixue Wang, Wenhua Tan

{"title":"RBM15-mediated N6-methyl adenosine (m6A) modification of EZH2 drives the epithelial-mesenchymal transition of cervical cancer","authors":"Ruixue Wang, Wenhua Tan","doi":"10.1615/critreveukaryotgeneexpr.2024052205","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024052205","url":null,"abstract":"RBM15 functions as an oncogene in multi-type cancers. However, the report on the roles of RBM15 in cervical cancer is limited. The purpose of this study was to investigate the potentials of RBM15 in cervical cancer. RT-qPCR was conducted to determine mRNA levels. Western was carried out to detect protein expression. CCK-8 and colony formation assays were carried out to determine cell proliferation. Scratch and transwell assays were carried out to determine cell migration and invasion. MeRIP assay was conducted to determine N6-methyl adenosine (m6A) levels. Luciferase assay was conducted to verify the m6A sites of EZH2 and binding sites between cc and promoter of FN1. ChIP assay was conducted to verify the interaction between EZH2 and FN1. RBM15 was upregulated in cervical cancer tissues and cells. Moreover, high levels of RBM15 predicted poor clinical outcomes of cervical cancer patients. RBM15 knockdown inhibited the proliferation and epithelial-mesenchymal transition (EMT) of cervical cancer cells. RBM15 promoted the m6A modification of EZH2 as well as its protein translation. Additionally, EZH2 bound to the promoter of fibronectin 1 (FN1) and EZH2-FN1 is the cascade downstream of RBM15. Overexpressed EZH2 antagonized the effects of RBM15 knockdown and promoted the aggressiveness of cervical cancer. In summary, RBM15/EZH2/FN1 signaling cascade induces the proliferation and EMT of cervical cancer. Therefore, RBM15/EZH2/FN1 signaling may be a promising strategy for cervical cancer.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139764428","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

SIAH1 promotes the pyroptosis of cardiomyocytes in diabetic cardiomyopathy via regulating IκB-α/NF-κB signaling SIAH1 通过调控 IκB-α/NF-κB 信号促进糖尿病心肌病中心肌细胞的脓毒症

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-02-01 DOI: 10.1615/critreveukaryotgeneexpr.2024052773

Jinbin Wu, Yaoming Yan

{"title":"SIAH1 promotes the pyroptosis of cardiomyocytes in diabetic cardiomyopathy via regulating IκB-α/NF-κB signaling","authors":"Jinbin Wu, Yaoming Yan","doi":"10.1615/critreveukaryotgeneexpr.2024052773","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024052773","url":null,"abstract":"Inflammation-mediated dysfunction of cardiomyocytes is the main cause of diabetic cardiomyopathy (DCM). The present study aimed to investigate the roles of SIAH1 in DCM. RT-qPCR was conducted to detect mRNA levels. ELISA was performed to detect cytokine release. Western blot was used to detect protein expression. LDH assay was used to determine cytotoxicity. In vitro ubiquitination assay was applied to determine the ubiquitination of IκB-α. TUNEL assay was conducted to determine cell death. Flow cytometry was applied for determining cardiomyocyte pyroptosis. The results showed that SIAH1 was overexpressed in human inflammatory cardiomyopathy. High expression of SIAH1 was associated with inflammatory response. SIAH1 was also overexpressed lipopolysaccharide (LPS)-induced inflammatory cardiomyopathy model in vitro. However, SIAH1 knockdown suppressed the inflammatory-related pyroptosis of cardiomyocytes. SIAH1 promoted the ubiquitination of IκB-α and activation of NF-κB signaling, which promoted the pyroptosis of cardiomyocytes. In conclusion, SIAH1 exacerbated the progression of human inflammatory cardiomyopathy via inducing the ubiquitination of IκB-α and activation of NF-κB signaling. Therefore, SIAH1/IκB-α/NF-κB signaling may be a potential target for human inflammatory cardiomyopathy.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139969659","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

SIAH2-mediated degradation of ACSL4 inhibits the anti-tumor activity of CD8+ T cells in hepatocellular carcinoma SIAH2 介导的 ACSL4 降解抑制 CD8+ T 细胞在肝细胞癌中的抗肿瘤活性

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-02-01 DOI: 10.1615/critreveukaryotgeneexpr.2024051981

Fangzheng Shu, Yuhua Shi, Xiangxiang Shan, Wenzhang Zha, Rengen Fan, Wanjiang Xue

{"title":"SIAH2-mediated degradation of ACSL4 inhibits the anti-tumor activity of CD8+ T cells in hepatocellular carcinoma","authors":"Fangzheng Shu, Yuhua Shi, Xiangxiang Shan, Wenzhang Zha, Rengen Fan, Wanjiang Xue","doi":"10.1615/critreveukaryotgeneexpr.2024051981","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024051981","url":null,"abstract":"SIAH2 function as an oncogene in various cancer. However, the roles of SIAH2 in hepatocellular carcinoma (HCC) is still unknown. This study aimed to investigate the roles of SIAH2 in HCC. Immunohistochemistry was used determine SIAH2 and ACSL4 expression in clinical samples. RT-qPCR was used to determine mRNA expression. Western blot assay was applied for determined protein expression. Ubiquitination assay was conducted for determining ubiquitination of ACSL4. Xenograft experiment was applied for determining tumor growth. Flow cytometry was applied to determine the functions of CD8+ T cells. SIAH2 expression was overexpressed in HCC tumors. High levels of SIAH2 predicted poor outcomes. However, SIAH2 knockdown promoted the proliferation of CD8+ T cells as well as promoted the ferroptosis of tumor cells, inhibiting tumor growth in HCC. ACSL4 is required for CD8+ T cell-mediated ferroptosis of HCC cells. However, SIAH2 induced ubiquitination of ACSL4 and inhibited its expression. Arachidonic acid and MEN synergistically promoted the immune checkpoint blockade. SIAH2-mediated inactivation of CD8+ T cells inhibits the ferroptosis of HCC. Therefore, targeting SIAH2 may be a promising strategy for HCC.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139764553","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

K-Homology Type Splicing Regulatory Protein: Mechanism of Action in Cancer and Immune Disorders. K同源型剪接调节蛋白：癌症和免疫疾病的作用机制。

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2023048085

Jonathan D Leavenworth, Nabiha Yusuf, Quamarul Hassan

引用次数: 0

miR-26b-5p Affects the Progression of Acute Myeloid Leukemia by Regulating the USP48-Mediated Wnt/β-Catenin Pathway miR-26b-5p 通过调控 USP48 介导的 Wnt/β-Catenin 通路影响急性髓性白血病的进展

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-01-01 DOI: 10.1615/critreveukaryotgeneexpr.2024049380

Yu Xie, Lin Tan, Kun Wu, Deyun Li, Chengping Li

{"title":"miR-26b-5p Affects the Progression of Acute Myeloid Leukemia by Regulating the USP48-Mediated Wnt/β-Catenin Pathway","authors":"Yu Xie, Lin Tan, Kun Wu, Deyun Li, Chengping Li","doi":"10.1615/critreveukaryotgeneexpr.2024049380","DOIUrl":"https://doi.org/10.1615/critreveukaryotgeneexpr.2024049380","url":null,"abstract":"Acute myeloid leukemia (AML) is a highly heterogeneous disease. Exploring the pathogenesis of AML is still an important topic in the treatment of AML. The expression levels of miR-26b-5p and USP48 were measured by qRT-PCR. The expression levels of related proteins were detected by Western blot. Cell proliferation and apoptosis were detected by CCK-8 and flow cytometry, respectively. Coimmunoprecipitation was used to examine the interaction between USP48 and Wnt5a. Bioinformatics analysis showed that high levels of miR-26b-5p and low levels of USP48 were associated with poor prognosis in AML. miR-26b-5p can negatively regulate the expression of USP48. Downregulation of miR-26b-5p inhibited EMT, cell viability and proliferation of AML cells and accelerated apoptosis. Furthermore, the influence of miR-26b-5p inhibition and USP48 knockdown on AML progression could be reversed by a Wnt/β-catenin signaling pathway inhibitor. This study revealed that miR-26b-5p regulates AML progression, possibly by targeting the USP48-mediated Wnt/β-catenin molecular axis to affect AML cell biological behavior.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139677531","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

HDAC1-mediated downregulation of NEU1 exacerbates the aggressiveness of cervical cancer HDAC1 介导的 NEU1 下调会加剧宫颈癌的侵袭性

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-01-01 DOI: 10.1615/critreveukaryotgeneexpr.2023051396

Nanzi Xie, Sisi Mei, Changlan Dai, Wei Chen

引用次数: 0

Methylation Regulation of LPCAT3 Improves Osteoarthritis by Regulating ACSL4 to Inhibit Chondrocyte Ferroptosis. LPCAT3的甲基化调控通过调节ACSL4抑制软骨细胞铁凋亡改善骨关节炎

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2023049244

Kaken Habaxi, Wei Wang, Maimaitiaili Taximaimaiti, Li Wang

{"title":"Methylation Regulation of LPCAT3 Improves Osteoarthritis by Regulating ACSL4 to Inhibit Chondrocyte Ferroptosis.","authors":"Kaken Habaxi, Wei Wang, Maimaitiaili Taximaimaiti, Li Wang","doi":"10.1615/CritRevEukaryotGeneExpr.2023049244","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2023049244","url":null,"abstract":"With the increasing aging population in China, the incidence rate of knee osteoarthritis is expected to rise annually. Therefore, we conducted a study to investigate the crucial role of LPCAT3 in osteoarthritis and its underlying mechanisms. We collected samples from normal volunteers (n = 12) and patients with osteoarthritis (n = 12) at our hospital. It was observed that LPCAT3 mRNA expression was reduced and positively correlated with IL-1β mRNA expression in patients with osteoarthritis. In a mouse model, LPCAT3 mRNA and protein expression were found to be suppressed. Furthermore, in an in vitro model, the enrichment level of LPCAT3 mRNA was inhibited by a specific m6A antibody through si-METTL3. Si-METTL3 also reduced the stability of LPCAT3 mRNA in the in vitro model. The inhibition of LPCAT3 was found to exacerbate osteoarthritis in the mouse model. Additionally, LPCAT3 was shown to reduce inflammation in the in vitro model. It was also observed that LPCAT3 reduced chondrocyte ferroptosis by inhibiting mitochondrial damage. LPCAT3 protein was found to interact with ACSL4 protein, and its up-regulation suppressed ACSL4 expression in the in vitro model. ACSL4 was identified as a target of LPCAT3 for suppressing mitochondrial damage in the in vitro model. In conclusion, this study demonstrates that LPCAT3 improves osteoarthritis by regulating ACSL4 to inhibit chondrocyte ferroptosis, thus providing a novel target for the treatment of osteoarthritis.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"67423974","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 ceRNA Mechanism of lncRNA MEG3/miR-21-5p/SPRY2 in Cell Proliferation and Apoptosis in Bladder Cancer. lncRNA MEG3/miR-21-5p/SPRY2在膀胱癌症细胞增殖和凋亡中的ceRNA机制。

IF 1.6 4区医学

Critical Reviews in Eukaryotic Gene Expression Pub Date : 2024-01-01 DOI: 10.1615/CritRevEukaryotGeneExpr.2023048011

Yangchun Hong, Zhen Li, Yixin Su, Hexian Pu, Xiuxiu Zhang

{"title":"The ceRNA Mechanism of lncRNA MEG3/miR-21-5p/SPRY2 in Cell Proliferation and Apoptosis in Bladder Cancer.","authors":"Yangchun Hong, Zhen Li, Yixin Su, Hexian Pu, Xiuxiu Zhang","doi":"10.1615/CritRevEukaryotGeneExpr.2023048011","DOIUrl":"10.1615/CritRevEukaryotGeneExpr.2023048011","url":null,"abstract":"Bladder cancer (BC) is the second most common genitourinary malignancy. Long noncoding RNA (lncRNA) is implicated in BC progression. This study delved into the underlying mechanism of lncRNA MEG3 in BC. Bioinformatics analysis predicted the expression of lncRNA MEG3, its association with the survival of BC patients, its subcellular localization, and its binding sites with miR-21-5p. Differentially expressed genes (DEGs) in the GSE13507 chip were analyzed using GEOexplorer, downstream targets of miR-21-5p were predicted from databases, and the overlapping genes were analyzed by the website Venny2.1 (https://bioinfogp.cnb.csic.es/tools/venny/index.html); their impacts on patient survival were analyzed by the Starbase database. The expression of SPRY2 and TGFBI associated with patient survival was analyzed in TCGA. RT-qPCR and western blot were performed to detect levels of MEG3, miR-21-5p, and SPRY2 in BC/SV-HUC-1 cells. Malignant biological behaviors of BC cells were detected using CCK8, flow cytometry, and Transwell assays. RNA pull-down and dual-luciferase assays were employed to verify the binding relationship of miR-21-5p with MEG3 and SPRY2. MEG3 was found to be lowly expressed in BC cells and mainly distributed in the cytoplasm. Over-expression of MEG3 was found to inhibit BC cell activity, promote apoptosis, and reduce invasion and migration. miR-21-5p was found to be highly expressed in BC cells, and its down-regulation was found to inhibit the malignant behavior of BC cells. Over-expression of miR-21-5p was found to reverse the effect of pcDNA3.1-MEG3 on BC cells. MEG3 was found to competitively bind to miR-21-5p as a ceRNA to promote SPRY2 levels. LncRNA MEG3 promotes SPRY2 expression by competitively binding to miR-21-5p, thereby inhibiting proliferation and promoting apoptosis of BC cells.","PeriodicalId":56317,"journal":{"name":"Critical Reviews in Eukaryotic Gene Expression","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41221452","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