Acta biochimica et biophysica Sinica最新文献_第9页

Significant biomarkers for predicting 1-month changes in IGF-1 in growth hormone-deficient children following r-hGH therapy. 预测生长激素缺乏症儿童接受r-hGH治疗后1个月IGF-1变化的重要生物标志物。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-06-07 DOI: 10.3724/abbs.2024089

Fei Liu, NokI Lei, Wunying Li, Yiwen Zheng, Liangjian Hu, Ronggui Hu, Wenli Lu, Yu S Huang

引用次数: 0

Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1. 通过靶向 Chl1，上调 miR-10a-5p 的表达可抑制神经干细胞的增殖和分化。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-06-05 DOI: 10.3724/abbs.2024078

Juan Zhang, Lihong Yang, Yuqing Sun, Li Zhang, Yufei Wang, Ming Liu, Xiujuan Li, Yuxiang Liang, Hong Zhao, Zhizhen Liu, Zhiyong Qiu, Ting Zhang, Jun Xie

{"title":"Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targeting Chl1.","authors":"Juan Zhang, Lihong Yang, Yuqing Sun, Li Zhang, Yufei Wang, Ming Liu, Xiujuan Li, Yuxiang Liang, Hong Zhao, Zhizhen Liu, Zhiyong Qiu, Ting Zhang, Jun Xie","doi":"10.3724/abbs.2024078","DOIUrl":"10.3724/abbs.2024078","url":null,"abstract":"Neural tube defects (NTDs) are characterized by the failure of neural tube closure during embryogenesis and are considered the most common and severe central nervous system anomalies during early development. Recent microRNA (miRNA) expression profiling studies have revealed that the dysregulation of several miRNAs plays an important role in retinoic acid (RA)-induced NTDs. However, the molecular functions of these miRNAs in NTDs remain largely unidentified. Here, we show that miR-10a-5p is significantly upregulated in RA-induced NTDs and results in reduced cell growth due to cell cycle arrest and dysregulation of cell differentiation. Moreover, the cell adhesion molecule L1-like ( Chl1) is identified as a direct target of miR-10a-5p in neural stem cells (NSCs) in vitro, and its expression is reduced in RA-induced NTDs. siRNA-mediated knockdown of intracellular Chl1 affects cell proliferation and differentiation similar to those of miR-10a-5p overexpression, which further leads to the inhibition of the expressions of downstream ERK1/2 MAPK signaling pathway proteins. These cellular responses are abrogated by either increased expression of the direct target of miR-10a-5p ( Chl1) or an ERK agonist such as honokiol. Overall, our study demonstrates that miR-10a-5p plays a major role in the process of NSC growth and differentiation by directly targeting Chl1, which in turn induces the downregulation of the ERK1/2 cascade, suggesting that miR-10a-5p and Chl1 are critical for NTD formation in the development of embryos.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to: TMEM106A transcriptionally regulated by promoter methylation is involved in invasion and metastasis of hepatocellular carcinoma. 更正：受启动子甲基化调控的 TMEM106A 转录参与了肝细胞癌的侵袭和转移。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-06-05 DOI: 10.3724/abbs.2022069C

Shiming Shi, Biao Wang, Jinglei Wan, Lina Song, Guiqi Zhu, Junxian Du, Luxi Ye, Qianqian Zhao, Jialiang Cai, Qing Chen, Kun Xiao, Jian He, Lei Yu, Zhi Dai

引用次数: 0

A PCR-independent, annealing-free cloning method for the insertion of short DNA fragments. 一种不依赖 PCR 的无退火克隆方法，用于插入短 DNA 片段。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-06-04 DOI: 10.3724/abbs.2024088

Linbo Li, Jin Yan, Yuan Qi, Zhenglong Xiang, Na Jiang, Tongkang Yuan, Zhenyi Wang, Yuan Wang, Huaizhe Zhan, Shiyi Liu, Li Zhao, Jing Xu, Xiaowei Lei, Yuxuan Liu, Gui Wang, Jiayang Xie, Zhenming Guo, Chunhai Cai, Shan Bian

引用次数: 0

Epigallocatechin-3-gallate inhibits osteogenic differentiation of vascular smooth muscle cells through the transcription factor JunB. 表没食子儿茶素-3-棓酸盐通过转录因子 JunB 抑制血管平滑肌细胞的成骨分化。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-06-03 DOI: 10.3724/abbs.2024060

Tiantian Li, Fei Fang, Hongmei Yin, Zhen Zhang, Xiangxiu Wang, Erxiang Wang, Hongchi Yu, Yang Shen, Guixue Wang, Weihong He, Xiaoheng Liu

{"title":"Epigallocatechin-3-gallate inhibits osteogenic differentiation of vascular smooth muscle cells through the transcription factor JunB.","authors":"Tiantian Li, Fei Fang, Hongmei Yin, Zhen Zhang, Xiangxiu Wang, Erxiang Wang, Hongchi Yu, Yang Shen, Guixue Wang, Weihong He, Xiaoheng Liu","doi":"10.3724/abbs.2024060","DOIUrl":"https://doi.org/10.3724/abbs.2024060","url":null,"abstract":"Medial arterial calcification (MAC) accompanying chronic kidney disease (CKD) leads to increased vessel wall stiffness, myocardial ischemia, heart failure, and increased cardiovascular morbidity and mortality. Unfortunately, there are currently no drugs available to treat MAC. The natural polyphenol epigallocatechin-3-gallate (EGCG) has been demonstrated to protect against cardiovascular disease; however, whether EGCG supplementation inhibits MAC in CKD remains unclear. In this study, we utilize a CKD-associated MAC model to investigate the effects of EGCG on vascular calcification and elucidate the underlying mechanisms involved. Our findings demonstrate that EGCG treatment significantly reduces calcium phosphate deposition and osteogenic differentiation of VSMCs in vivo and in vitro in a dose-dependent manner. In addition, through RNA sequencing (RNA-seq) analysis, we show a significant activation of the transcription factor JunB both in CKD mouse arteries and in osteoblast-like VSMCs. Notably, EGCG effectively suppresses CKD-associated MAC by inhibiting the activity of JunB. In addition, overexpression of JunB can abolish while knockdown of JunB can enhance the inhibitory effect of EGCG on the osteogenic differentiation of VSMCs. Furthermore, EGCG supplementation inhibits MAC in CKD via modulation of the JunB-dependent Ras/Raf/MEK/ERK signaling pathway. In conclusion, our study highlights the potential therapeutic value of EGCG for managing CKD-associated MAC, as it mitigates this pathological process through targeted inactivation of JunB.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Citronellal improves endothelial dysfunction by affecting the stability of the GCH1 protein. 香茅醛通过影响 GCH1 蛋白的稳定性来改善内皮功能障碍。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-06-03 DOI: 10.3724/abbs.2024086

Yaqi Guo, Huadong Que, Bulei Chen, Chunyan Chao, Shanshan Li, Shuang Guo, Yaling Yin, Huanhuan Wang, Moli Zhu, Peng Li

{"title":"Citronellal improves endothelial dysfunction by affecting the stability of the GCH1 protein.","authors":"Yaqi Guo, Huadong Que, Bulei Chen, Chunyan Chao, Shanshan Li, Shuang Guo, Yaling Yin, Huanhuan Wang, Moli Zhu, Peng Li","doi":"10.3724/abbs.2024086","DOIUrl":"10.3724/abbs.2024086","url":null,"abstract":"Endothelial dysfunction (ED) serves as the pathological basis for various cardiovascular diseases. Guanosine triphosphate cyclopyrrolone 1 (GCH1) emerges as a pivotal protein in sustaining nitric oxide (NO) production within endothelial cells, yet it undergoes degradation under oxidative stress, contributing to endothelial cell dysfunction. Citronellal (CT), a monoterpenoid, has been shown to ameliorate endothelial dysfunction induced by in atherosclerosis rats. However, whether CT can inhibit the degradation of GCH1 protein is not clear. It has been reported that ubiquitination may play a crucial role in regulating GCH1 protein levels and activities. However, the specific E3 ligase for GCH1 and the molecular mechanism of GCH1 ubiquitination remain unclear. Using data-base exploration analysis, we find that the levels of the E3 ligase Smad-ubiquitination regulatory factor 2 (Smurf2) negatively correlate with those of GCH1 in vascular tissues and HUVECs. We observe that Smurf2 interacts with GCH1 and promotes its degradation via the proteasome pathway. Interestingly, ectopic Smurf2 expression not only decreases GCH1 levels but also reduces cell proliferation and reactive oxygen species (ROS) levels, mostly because of increased GCH1 accumulation. Furthermore, we identify BH 4/eNOS as downstream of GCH1. Taken together, our results indicate that CT can obviously improve vascular endothelial injury in Type 1 diabetes mellitus (T1DM) rats and reverse the expressions of GCH1 and Smurf2 proteins in aorta of T1DM rats. Smurf2 promotes ubiquitination and degradation of GCH1 through proteasome pathway in HUVECs. We conclude that the Smurf2-GCH1 interaction might represent a potential target for improving endothelial injury.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11322867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PACSIN1 promotes immunosuppression in gastric cancer by degrading MHC-I. PACSIN1 通过降解 MHC-I 促进胃癌的免疫抑制。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-05-31 DOI: 10.3724/abbs.2024059

Zhu Liu, Xin Li, Ali Muhammad, Qiannan Sun, Qi Zhang, Yang Wang, Yong Wang, Jun Ren, Daorong Wang

{"title":"PACSIN1 promotes immunosuppression in gastric cancer by degrading MHC-I.","authors":"Zhu Liu, Xin Li, Ali Muhammad, Qiannan Sun, Qi Zhang, Yang Wang, Yong Wang, Jun Ren, Daorong Wang","doi":"10.3724/abbs.2024059","DOIUrl":"10.3724/abbs.2024059","url":null,"abstract":"Gastric cancer (GC) is a common gastrointestinal system malignancy. PACSIN1 functions as an oncogene in various cancers. This study aims to investigate the potential of PACSIN1 as a target in GC treatment. Gene expression is determined by RT-qPCR, immunofluorescence staining, and immunohistochemistry assay. FISH is performed to determine the colocalization of PACSIN1 and the major histocompatibility complex (MHC-I). Cytokine release and cell functions are analyzed by flow cytometry. In vivo assays are also conducted. Histological analysis is performed using H&E staining. The results show that PACSIN1 is overexpressed in GC patients, especially in those with immunologically-cold tumors. A high level of PACSIN1 is associated with poor prognosis. PACSIN1 deficiency inhibits autophagy but increases antigen presentation in GC cells. Moreover, PACSIN1 deficiency inhibits the lysosomal fusion and selective autophagy of MHC-I, increases CD8 + T-cell infiltration, and suppresses tumor growth and liver metastasis in vivo. Additionally, PACSIN1 knockout enhances the chemosensitivity of cells to immune checkpoint blockade. In summary, PACSIN1 mediates lysosomal fusion and selective autophagy of MHC-I and suppresses antigen presentation and CD8 + T-cell infiltration, thus inhibiting antitumor immunity in GC.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141199229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inducible Fgf13 ablation alleviates cardiac fibrosis via regulation of microtubule stability. 诱导性 Fgf13 消融可通过调节微管稳定性减轻心脏纤维化。

IF 3.7 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-05-31 DOI: 10.3724/abbs.2024075

Cong Wang, Xiangchong Wang, Yiyi Zhang, Yuan Mi, Yanxue Han, Yaxin Zhi, Ran Zhao, Nanqi Cui, Qianli Ma, Huaxing Zhang, Dazhong Xue, Ruoyang Qiao, Jiabing Han, Yulou Yu, Jiaxuan Li, Mohammed Shaiea, Demin Liu, Guoqiang Gu, Chuan Wang

{"title":"Inducible Fgf13 ablation alleviates cardiac fibrosis via regulation of microtubule stability.","authors":"Cong Wang, Xiangchong Wang, Yiyi Zhang, Yuan Mi, Yanxue Han, Yaxin Zhi, Ran Zhao, Nanqi Cui, Qianli Ma, Huaxing Zhang, Dazhong Xue, Ruoyang Qiao, Jiabing Han, Yulou Yu, Jiaxuan Li, Mohammed Shaiea, Demin Liu, Guoqiang Gu, Chuan Wang","doi":"10.3724/abbs.2024075","DOIUrl":"https://doi.org/10.3724/abbs.2024075","url":null,"abstract":"Fibroblast growth factor (FGF) isoform 13, a distinct type of FGF, boasts significant potential for therapeutic intervention in cardiovascular dysfunctions. However, its impact on regulating fibrosis remains unexplored. This study aims to elucidate the role and mechanism of FGF13 on cardiac fibrosis. Here, we show that following transverse aortic constriction (TAC) surgery, interstitial fibrosis and collagen content increase in mice, along with reduced ejection fraction and fractional shortening, augmented heart mass. However, following Fgf13 deletion, interstitial fibrosis is decreased, ejection fraction and fractional shortening are increased, and heart mass is decreased, compared with those in the TAC group. Mechanistically, incubation of cardiac fibroblasts with transforming growth factor β (TGFβ) increases the expressions of types I and III collagen proteins, as well as α-smooth muscle actin (α-SMA) proteins, and enhances fibroblast proliferation and migration. In the absence of Fgf13, the expressions of these proteins are decreased, and fibroblast proliferation and migration are suppressed, compared with those in the TGFβ-stimulated group. Overexpression of FGF13, but not FGF13 mutants defective in microtubule binding and stabilization, rescues the decrease in collagen and α-SMA protein and weakens the proliferation and migration function of the Fgf13 knockdown group. Furthermore, Fgf13 knockdown decreases ROCK protein expression via microtubule disruption. Collectively, cardiac Fgf13 knockdown protects the heart from fibrosis in response to haemodynamic stress by modulating microtubule stabilization and ROCK signaling pathway.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.7,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Development of an alcoholic liver disease model for drug evaluation from human induced pluripotent stem cell-derived liver organoids. 从人类诱导多能干细胞衍生的肝脏器官组织中开发酒精性肝病模型，用于药物评估。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-05-30 DOI: 10.3724/abbs.2024074

Zhiwei Feng, Bingrui Zhou, Qizhi Shuai, Yunliang Wei, Ning Jin, Xiaoling Wang, Hong Zhao, Zhizhen Liu, Jun Xu, Jianbing Mu, Jun Xie

{"title":"Development of an alcoholic liver disease model for drug evaluation from human induced pluripotent stem cell-derived liver organoids.","authors":"Zhiwei Feng, Bingrui Zhou, Qizhi Shuai, Yunliang Wei, Ning Jin, Xiaoling Wang, Hong Zhao, Zhizhen Liu, Jun Xu, Jianbing Mu, Jun Xie","doi":"10.3724/abbs.2024074","DOIUrl":"10.3724/abbs.2024074","url":null,"abstract":"Alcoholic liver disease (ALD) poses a significant health challenge, so comprehensive research efforts to improve our understanding and treatment strategies are needed. However, the development of effective treatments is hindered by the limitation of existing liver disease models. Liver organoids, characterized by their cellular complexity and three-dimensional (3D) tissue structure closely resembling the human liver, hold promise as ideal models for liver disease research. In this study, we use a meticulously designed protocol involving the differentiation of human induced pluripotent stem cells (hiPSCs) into liver organoids. This process incorporates a precise combination of cytokines and small molecule compounds within a 3D culture system to guide the differentiation process. Subsequently, these differentiated liver organoids are subject to ethanol treatment to induce ALD, thus establishing a disease model. A rigorous assessment through a series of experiments reveals that this model partially recapitulates key pathological features observed in clinical ALD, including cellular mitochondrial damage, elevated cellular reactive oxygen species (ROS) levels, fatty liver, and hepatocyte necrosis. In addition, this model offers potential use in screening drugs for ALD treatment. Overall, the liver organoid model of ALD, which is derived from hiPSC differentiation, has emerged as an invaluable platform for advancing our understanding and management of ALD in clinical settings.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11532202/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

COL5A2 drives regorafenib resistance-induced metastatic phenotype via reducing LIFR expression in hepatocellular carcinoma. COL5A2通过降低肝细胞癌中LIFR的表达，驱动瑞戈非尼耐药诱导的转移表型。

IF 3.3 2区生物学

Acta biochimica et biophysica Sinica Pub Date : 2024-05-30 DOI: 10.3724/abbs.2024058

Shaoqin Zhang, Xuezhen Xue, Fengdan Chen, Yahan Yang, Nan Zhang, Yan Chen, Wenda Wu, Jichuang Wang, Ning Zheng

{"title":"COL5A2 drives regorafenib resistance-induced metastatic phenotype via reducing LIFR expression in hepatocellular carcinoma.","authors":"Shaoqin Zhang, Xuezhen Xue, Fengdan Chen, Yahan Yang, Nan Zhang, Yan Chen, Wenda Wu, Jichuang Wang, Ning Zheng","doi":"10.3724/abbs.2024058","DOIUrl":"10.3724/abbs.2024058","url":null,"abstract":"Systemic therapies, the ultimate strategies for patients with advanced hepatocellular carcinoma (HCC), are suffering from serious clinical challenges, such as the occurrence and development of drug resistance. Treatment resistance aggravates tumor progression partly by inducing tumor metastasis. Regorafenib-resistant HCC cells exhibit a highly striking metastatic phenotype, but the detailed mechanisms underlying these aggressive behaviors remain elusive. Here, we conduct transcriptome sequencing analysis to identify COL5A2 as a crucial driver of the metastatic characteristics of regorafenib-resistant HCC cells. COL5A2 is aberrantly highly expressed in resistant cells, and its genetic depletion significantly suppresses proliferation, migration, invasion, vasculogenic mimicry (VM) formation and lung metastasis in vitro and in vivo, concomitant with the downregulation of VE-cadherin, EphA2, Twist1, p-p38 and p-STAT3 expressions. LIFR is confirmed to be an essential downstream molecule of COL5A2, and its expression is observably elevated by COL5A2 depletion. Ectopic overexpression of LIFR drastically attenuates the proliferation, migration, invasion and VM of regorafenib-resistant cells and represses the expressions of VM-related molecules and the activation of p38/STAT3 signaling pathway. Interestingly, rescue experiments show that the inhibition of the above aggressive features of resistant cells by COL5A2 loss is clearly alleviated by silencing of LIFR. Collectively, our results reveal that COL5A2 promotes the ability of regorafenib-resistant HCC cells to acquire a metastatic phenotype by attenuating LIFR expression and suggest that therapeutic regimens targeting the COL5A2/LIFR axis may be beneficial for HCC patients with therapeutic resistance.","PeriodicalId":6978,"journal":{"name":"Acta biochimica et biophysica Sinica","volume":null,"pages":null},"PeriodicalIF":3.3,"publicationDate":"2024-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11322875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141178651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0