General physiology and biophysics最新文献_第4页

lncRNA MEG3 promotes hypoxia/reoxygenation-induced ferroptosis and cell injury in H9C2 cells through regulating the miR-22/TP53 axis. lncRNA MEG3通过调节miR-22/TP53轴促进缺氧/再氧诱导的H9C2细胞铁凋亡和细胞损伤。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2026-03-01 DOI: 10.4149/gpb_2025048

Guangyu Ma, Hairui Jiang, Meina Li, Caijie Li, Ningning Zhang

{"title":"lncRNA MEG3 promotes hypoxia/reoxygenation-induced ferroptosis and cell injury in H9C2 cells through regulating the miR-22/TP53 axis.","authors":"Guangyu Ma, Hairui Jiang, Meina Li, Caijie Li, Ningning Zhang","doi":"10.4149/gpb_2025048","DOIUrl":"10.4149/gpb_2025048","url":null,"abstract":"Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) is crucial in cerebral ischemia/reperfusion and cardiovascular cell injury. However, the effect of lncRNA MEG3 on ferroptosis due to myocardial ischemia/reperfusion is unknown. Hypoxia/reoxygenation (H/R) H9C2 cell model was constructed. qRT-PCR detected MEG3, miR-22 and tumor protein 53 (TP53) expression, and the location of MEG3 was assessed by RNA FISH. Dual luciferase assay was employed to verify whether lncRNA MEG3 targets and regulates miR-22. Cell counting kit-8 assay and EdU staining assessed cell proliferation, and flow cytometry assessed apoptosis rate. The FerroOrange fluorescent probe and Fe2+ assay kit were used to detect Fe2+ levels, and different kits to determine oxidative stress and inflammatory factors levels. Ferroptosis-related proteins levels were assessed via Western blot. H9C2 cell viability and proliferation were reduced, while apoptosis and pro-inflammatory factors were elevated after H/R. lncRNA MEG3 was upregulated in H/R-treated H9C2 cells, overexpression MEG3 increased Fe2+ and oxidative stress levels, up-regulated ferroptosis-related proteins, and knockdown MEG3 reversed the above metrics. Additionally, MEG3 regulated miR-22/TP53 axis, silencing miR-22 promoted H9C2 cell injury and ferroptosis, whereas overexpression miR-22 increased the protective impact of knockdown MEG3 on H9C2 cells. lncRNA MEG3 promotes ferroptosis caused by H/R by modulating miR-22/TP53 in H9C2 cells.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 2","pages":"191-206"},"PeriodicalIF":1.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

The lncRNA SNHG9, an oncogenic regulator, stabilizes PRMT7 by binding to PTBP1 in the progression of colorectal cancer. lncRNA SNHG9是一种致癌调节剂，在结直肠癌的进展中通过与PTBP1结合来稳定PRMT7。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2026-03-01 DOI: 10.4149/gpb_2025045

Chengbai Liang

{"title":"The lncRNA SNHG9, an oncogenic regulator, stabilizes PRMT7 by binding to PTBP1 in the progression of colorectal cancer.","authors":"Chengbai Liang","doi":"10.4149/gpb_2025045","DOIUrl":"10.4149/gpb_2025045","url":null,"abstract":"Long noncoding RNAs (lncRNAs), widely regarded as nonprotein-coding transcripts longer than 200 nucleotides in length, play active roles in tumorigenesis, including in colorectal cancer (CRC). The abnormally elevated lncRNA small nucleolar RNA host gene 9 (SNHG9) in CRC samples was observed in The Cancer Genome Atlas (TCGA) database. However, the biological role and potential mechanism of SNHG9 in CRC development remain elusive. Herein, 49 paired CRC tissues and matched adjacent normal tissues were obtained to examine SNHG9 levels. Biological functions related to cell proliferation, migration and invasion were evaluated using CCK-8, colony formation, and Transwell assays and western blot analysis. RNA pull-down and RNA immunoprecipitation (RIP) assays were used to verify the SNHG9/PTBP1/PRMT7 regulatory axis. Interestingly, our data revealed that increasing levels of SNHG9 in CRC tissues and cells were positively correlated with poor prognosis and tumour metastasis, while depletion of SNHG9 caused the suppression of cell proliferation, migration, and invasion. Moreover, cytoplasmic SNHG9 enhanced the mRNA stability of PRMT7 by directly binding to PTBP1 through the \"lncRNA‒RNA binding protein (RBP)\" complex. The regulatory function of SNHG9 on PRMT7 was also validated via rescue functional assays. In summary, our data demonstrated that SNHG9 may play an oncogenic role in CRC tumorigenesis by stabilizing PRMT7 by recruiting PTBP1. This could be a prognostic biomarker and therapeutic target for CRC.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 2","pages":"167-178"},"PeriodicalIF":1.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148224403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Determining the effects of SGLT2 inhibitor on breast cancer cell migration and clonogenicity - a pilot study. 确定SGLT2抑制剂对乳腺癌细胞迁移和克隆性的影响-一项初步研究。

IF 1.3 4区生物学

General physiology and biophysics Pub Date : 2026-03-01 DOI: 10.4149/gpb_2025044

Vincent Lučanský, Ivana Baranová, Iryna Samec, Martin Jozef Péč, Renata Péčová, Marek Samec

引用次数: 0

Platelet-rich miR-21 is a predictive biomarker in osteosarcoma and promotes osteosarcoma cell malignancyM. 富血小板的miR-21是骨肉瘤的预测性生物标志物，可促进骨肉瘤细胞恶性m。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025037

Xi'an Pan, Shishi Dong, Farui Sun, Yuanjin Zhang, Guofu Zhang, Jun Li, Bingxia Liu

{"title":"Platelet-rich miR-21 is a predictive biomarker in osteosarcoma and promotes osteosarcoma cell malignancyM.","authors":"Xi'an Pan, Shishi Dong, Farui Sun, Yuanjin Zhang, Guofu Zhang, Jun Li, Bingxia Liu","doi":"10.4149/gpb_2025037","DOIUrl":"10.4149/gpb_2025037","url":null,"abstract":"Platelet-derived microRNAs (miRNAs) are regarded as diagnostic biomarkers as well as potent regulators of cancer development. The expression of miR-21, a vital miRNA, is elevated in the tumor tissues of osteosarcoma (OS) patients. However, platelet-derived miR-21 in OS is unknown. Here, we found that the level of miR-21 is increased in the serum of OS patients. The miR-21 level is associated with advanced tumor stages and poorer clinical outcomes in OS patients. Moreover, platelet-derived microvesicles (PMVs) from OS patients (OS-PMVs) significantly enhanced the miR-21 profile in MG63 OS cells. Functional assays revealed that the proliferation and migration of MG63 cells were promoted by OS-PMV incubation or the transfection of miR-21 mimics, whereas the sensitivity of MG63 cells to methotrexate (MTX), doxorubicin (ADM), and cisplatin (DDP) was reduced. However, inhibiting miR-21 partially reversed the OS-PMV-mediated effects. Furthermore, programmed cell death 4 (PDCD4) was identified as a potential target of miR-21 in OS. miR-21 considerably inhibited PDCD4 expression in MG63 cells and reversed the antitumor effects mediated by PDCD4 overexpression. In conclusion, our results suggest that platelet-rich miR-21 may promote the development of OS by targeting PDCD4.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 1","pages":"77-91"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Exploring the target points and mechanisms of Compound Danshen Dripping Pills in treating diabetic nephropathy based on network pharmacology and molecular docking technology. 基于网络药理学和分子对接技术探索复方丹参滴丸治疗糖尿病肾病的靶点及作用机制。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025034

Zhengju Du, Lidan Zhang, Ju Ran, Lisha Gao, Hongrong Chen, Honggang Ni

{"title":"Exploring the target points and mechanisms of Compound Danshen Dripping Pills in treating diabetic nephropathy based on network pharmacology and molecular docking technology.","authors":"Zhengju Du, Lidan Zhang, Ju Ran, Lisha Gao, Hongrong Chen, Honggang Ni","doi":"10.4149/gpb_2025034","DOIUrl":"10.4149/gpb_2025034","url":null,"abstract":"Diabetic nephropathy is a formidable complication arising from diabetes. Compound Danshen Dripping Pills (CDDP) has demonstrated remarkable efficacy in managing diabetic retinopathy. Our study integrates network pharmacology and molecular docking methodologies to explore the therapeutic targets and mechanisms of CDDP in diabetic nephropathy. We systematically retrieved compounds and their corresponding target molecules associated with CDDP from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) and UniProt databases. Our exhaustive analysis revealed 76 bioactive compounds and 203 potential targets for CDDP. Through meticulous Protein-Protein Interaction network analysis, we narrowed down on ten pivotal targets central to the therapeutic effects. Functional assessments illuminated the multifaceted impact of CDDP on metabolic homeostasis, inflammatory responses, oxidative stress modulation, and apoptotic regulation, implicating pathways such as lipid metabolism, atherosclerotic processes, and Advanced Glycation End-products receptor for Advanced Glycation End-products (AGE-RAGE) signaling cascade. Molecular docking assays further substantiated these findings by demonstrating a robust binding affinity between the bioactive constituents and their respective molecular targets. In conclusions, this study forecasts the complex interplay of components, therapeutic targets, and modulated pathways involved in CDDP's therapeutic intervention in diabetic nephropathy.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 1","pages":"19-31"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

lincRNA-p21 inhibits foam cell formation and regulates cholesterol uptake and efflux in macrophages through the PKCδ/Akt/Erk and PPARγ/LXRα pathways. lincRNA-p21通过PKCδ/Akt/Erk和PPARγ/LXRα途径抑制泡沫细胞形成，调节巨噬细胞胆固醇摄取和外排。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025040

Chao He, Wei Yang, Fei Zhou, Lin Teng, Hui Wu, Zhuli Guo, Jiawang Ding, Jing Zhang, Jian Yang, Song Li

{"title":"lincRNA-p21 inhibits foam cell formation and regulates cholesterol uptake and efflux in macrophages through the PKCδ/Akt/Erk and PPARγ/LXRα pathways.","authors":"Chao He, Wei Yang, Fei Zhou, Lin Teng, Hui Wu, Zhuli Guo, Jiawang Ding, Jing Zhang, Jian Yang, Song Li","doi":"10.4149/gpb_2025040","DOIUrl":"10.4149/gpb_2025040","url":null,"abstract":"Impairment in cholesterol uptake and efflux is the main reason contributing to foam cell formation, which is a marker and key step in the atherosclerotic process. Overexpression of long intergenic non-coding RNA-p21 (lincRNA-p21) was reported to alleviate the development of atherosclerosis. However, whether lincRNA-p21 exerts an antiatherogenic function by alleviating lipid metabolism dysfunction and foam cell formation remains unknown. In our study, human THP-1 monocytes were stimulated for 48 h by phorbol 12-myristate-13-acetate (PMA) to differentiate into macrophages, and THP-1-derived macrophages were further treated for 24 h with oxidized low-density lipoprotein (ox-LDL) to differentiate into foam cells. THP‑1 macrophage-derived foam cells were transfected with si-NC/si-lincRNA-p21 or LV-NC/LV-lincRNA-p21 for 48 h to knock down or overexpress lincRNA-p21. lincRNA-p21 expression was reduced in THP-1-derived macrophages after ox-LDL treatment. lincRNA-p21 knockdown promoted lipid uptake and accumulation and inhibited cholesterol efflux in ox-LDL-treated THP-1 macrophages, while lincRNA-p21 overexpression exerted an opposite effect on cholesterol influx and efflux. Importantly, lincRNA-p21 attenuated cholesterol influx by suppressing the PKCδ/Akt/Erk/SR-A/CD36 pathway and enhanced cholesterol efflux by promoting the PPARγ/LXRα/ABCA1/ABCG1 pathway in foam cells derived from THP-1 macrophages.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 1","pages":"107-120"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Silencing IL2RB attenuates abdominal aortic aneurysm-related pathology in experimental models by partially restoring mitochondrial homeostasis. 在实验模型中，沉默IL2RB通过部分恢复线粒体稳态减轻腹主动脉瘤相关病理。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025039

Pang Li, Hao Zhang, Jinfu Huang, Yijing Gao

{"title":"Silencing IL2RB attenuates abdominal aortic aneurysm-related pathology in experimental models by partially restoring mitochondrial homeostasis.","authors":"Pang Li, Hao Zhang, Jinfu Huang, Yijing Gao","doi":"10.4149/gpb_2025039","DOIUrl":"10.4149/gpb_2025039","url":null,"abstract":"Abdominal aortic aneurysm (AAA) remains a life-threatening vascular disease with limited therapeutic options. The role of interleukin-2 receptor subunit beta (IL2RB) in AAA via mitochondrial dysfunction is unclear. In this study, integrated bioinformatics analyses identified IL2RB as a key gene. In a rat AAA model and angiotensin II-stimulated vascular smooth muscle cells (VSMCs), IL2RB was upregulated and associated with mitochondrial impairment. IL2RB knockdown attenuated aortic dilation, reduced elastic fiber degradation (decreased by 45%), restored adenosine triphosphate (ATP) production (increased by 126.9%), suppressed interleukin-6 (decreased by 49.3%) and tumor necrosis factor-alpha (decreased by 51.8%) release, and decreased malondialdehyde (reduced by 47.7%) and reactive oxygen species (reduced by 38.5%) production in the rat model. In VSMCs, silencing IL2RB rescued angiotensin II-induced ATP depletion, preserved mitochondrial membrane potential, and reduced apoptosis. Mechanistically, IL2RB knockdown downregulated dynamin-related protein 1, and upregulated mitofusin 1 and parkin RBR E3 ubiquitin protein ligase. IL2RB knockdown mitigates AAA progression by restoring mitochondrial homeostasis and suppressing inflammation, identifying IL2RB as a potential therapeutic target for AAA.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 1","pages":"1-18"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

lncRNA H19 contributes to sevoflurane-induced neuronal death in SH-SY5Y cells via ACSL4-mediated ferroptosis pathway. lncRNA H19通过acsl4介导的铁下垂途径参与七氟醚诱导的SH-SY5Y细胞神经元死亡。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025025

Lixin Liu, Zhaoping Xue, Yan Liu, Ying Liu

{"title":"lncRNA H19 contributes to sevoflurane-induced neuronal death in SH-SY5Y cells via ACSL4-mediated ferroptosis pathway.","authors":"Lixin Liu, Zhaoping Xue, Yan Liu, Ying Liu","doi":"10.4149/gpb_2025025","DOIUrl":"10.4149/gpb_2025025","url":null,"abstract":"Sevoflurane induces neurotoxicity and cognitive impairment, with long noncoding RNAs (lncRNAs) playing key roles in nervous system diseases. This study explored lncRNA H19's function in sevoflurane-induced neurotoxicity. SH-SY5Y cell viability and apoptosis were assessed via CCK8 and TUNEL assays. Gene expression was measured by RT-qPCR, while reactive oxygen species (ROS), malondialdehyde (MDA), glutathione (GSH), and iron levels were quantified. Subcellular fractionation determined H19 localization, and luciferase assays confirmed H19/miR-20a-5p and miR-20a-5p/Acyl-CoA synthetase long chain family member 4 (ACSL4) interactions. Western blot analyzed ACSL4, apoptosis-, and ferroptosis-related proteins. The results showed that sevoflurane reduced viability, promoted apoptosis and ferroptosis, and upregulated H19 and ACSL4. H19 knockdown mitigated neurotoxicity by restoring viability, GSH, solute carrier family 7 member 11 (SLC7A11), and glutathione peroxidase 4 (GPX4), while reducing apoptosis, MDA, ROS, and iron. Mechanistically, H19 sponged miR-20a-5p to elevate ACSL4. Rescue assays showed miR-20a-5p inhibition or ACSL4 overexpression reversed H19 silencing's protective effects. Thus, H19 depletion alleviates sevoflurane-induced neuronal damage via the miR-20a-5p/ACSL4 axis, suggesting a potential therapeutic target.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 1","pages":"93-105"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Homocysteine affects the excitability of cultured thalamic neurons to a minor extent. 同型半胱氨酸对培养的丘脑神经元的兴奋性影响较小。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025047

Katarina Ondacova, Matus Tomko, Lubica Lacinova

引用次数: 0

Exosomal miR-147-3p regulates the growth of mouse bronchial epithelial cells and asthma progression via targeting RUNX3: a pilot study. 外泌体miR-147-3p通过靶向RUNX3调节小鼠支气管上皮细胞的生长和哮喘进展：一项初步研究

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2026-01-01 DOI: 10.4149/gpb_2025031

Xun Huang, Qi Zuo, Yuyun Yuan, Sihong Huang, Yantao Zhang, Yiyun Shen

{"title":"Exosomal miR-147-3p regulates the growth of mouse bronchial epithelial cells and asthma progression via targeting RUNX3: a pilot study.","authors":"Xun Huang, Qi Zuo, Yuyun Yuan, Sihong Huang, Yantao Zhang, Yiyun Shen","doi":"10.4149/gpb_2025031","DOIUrl":"10.4149/gpb_2025031","url":null,"abstract":"Exosomes are endogenous vesicles that transport microRNAs (miRNAs), thereby mediating intercellular communication. This study was assigned to expound the regulatory role of exosomal miR-147-3p in asthma progression. The ovalbumin-mediated murine model of asthma was established to obtain bronchoalveolar lavage fluid (BALF), and exosomes were isolated by ultrafiltration centrifugation. Differential expression of exosomal miRNA and mRNA was analyzed by RT-PCR. Dual-luciferase was utilized to validate potential binding between key miRNAs and target genes. Additionally, the impact of miRNA mimics and BALF-exosomes on growth of bronchial epithelial cells (BECs) was assessed, followed by RT-qPCR and Western blot. Ovalbumin exposure induced asthma phenotypes in mice. Notably, miR-147-3p and miR-146b-5p were markedly elevated in BALF exosomes from asthmatic mice, whereas miR-98-5p and RUNX3 were markedly decreased. Luciferase assay confirmed the direct binding of miR-147-3p to RUNX3 mRNA 3' UTR. Furthermore, PKH26-labeled exosomes were internalized by BECs. Asthmatic BALF-exosomes or miR-147-3p mimics reduced cell viability and migration while promoting apoptosis. This phenomenon could be reversed by miR-147-3p inhibition. miR-147-3p overexpression or asthmatic BAF-exosomes suppressed RUNX3 protein and mRNA expression. BALF-derived exosomal miR-147-3p modulated behaviors of BECs via targeting RUNX3, suggesting its potential as a therapeutic target and biomarker for asthma pathogenesis.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"45 1","pages":"63-75"},"PeriodicalIF":1.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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