Molecular and Cellular Biology最新文献_第7页

Paeonol Ameliorates Gastric Mucosal Enterosis and Dysplasia Associated with Chronic Atrophic Gastritis by Modulating the JAK2/STAT3 Pathway. 丹皮酚通过调节JAK2/STAT3通路改善慢性萎缩性胃炎相关的胃黏膜肠病和发育不良

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-03-19 DOI: 10.1080/10985549.2026.2638205

Lei Zhang, Lei Zou

{"title":"Paeonol Ameliorates Gastric Mucosal Enterosis and Dysplasia Associated with Chronic Atrophic Gastritis by Modulating the JAK2/STAT3 Pathway.","authors":"Lei Zhang, Lei Zou","doi":"10.1080/10985549.2026.2638205","DOIUrl":"10.1080/10985549.2026.2638205","url":null,"abstract":"Paeonol (Pae) exhibits potent anti-inflammatory and antitumor effects. Chronic atrophic gastritis (CAG) is considered a gastric precancerous lesion, and the JAK2/STAT3 pathway plays a key role in gastrointestinal inflammation and tumorigenesis. Whether Pae ameliorates CAG by regulating this pathway remains unclear. A 1-methyl-3-nitro-1-nitrosoguanidine (MNNG)-induced malignant transformed cell (MC) model and a CAG rat model were established. The malignant biological behaviors of MC cells were assessed using the Cell Counting Kit-8 (CCK-8) assay, clone formation, and Transwell assays. Gastric histopathological changes were examined by pathological staining, inflammatory factors and gastric mucosa-associated factors were detected via enzyme-linked immunosorbent assay (ELISA). Inflammation, proliferation, epithelial-mesenchymal transition (EMT), and the JAK2/STAT3 pathway-related protein expression was analyzed by Western blotting. MC cells exhibited enhanced proliferation, migration, invasion, and EMT, all of which were significantly suppressed by Pae treatment. CAG rats showed severe gastric mucosal damage, intestinal metaplasia, collagen fiber disorganization, and increased Ki-67 expression. Pae treatment alleviated histopathological injury, reduced inflammatory factor levels, and promoted gastric mucosa-associated factor synthesis. Furthermore, Pae markedly inhibited the JAK2/STAT3 pathway in MC cells and gastric tissues. In conclusion, Pae suppresses malignant transformation and alleviates gastric histopathological injury in CAG by modulating the JAK2/STAT3 pathway.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"655-672"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147481032","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

Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage. 人lncRNA， hLinfRNA7 （IDO1-AS）调节巨噬细胞中细胞因子表达、色氨酸分解代谢和炎症反应。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2026-01-01 Epub Date: 2026-06-05 DOI: 10.1080/10985549.2026.2678458

Ashcharya Rishi, Prarthana Guha, Nagashree Bhat, Avisankar Chini, Pavan K Gondrala, Subhrangsu S Mandal

{"title":"Human lncRNA, hLinfRNA7 (IDO1-AS) Regulates Cytokine Expression, Tryptophan Catabolism, and Inflammatory Response in Macrophage.","authors":"Ashcharya Rishi, Prarthana Guha, Nagashree Bhat, Avisankar Chini, Pavan K Gondrala, Subhrangsu S Mandal","doi":"10.1080/10985549.2026.2678458","DOIUrl":"10.1080/10985549.2026.2678458","url":null,"abstract":"Noncoding RNAs are emerging players in cell signaling and diseases. Recently, we discovered a series of novel lncRNAs that are critical players in inflammation. Here, we demonstrate that hLinfRNA7, a long human noncoding inflammation-associated RNA 7 (also termed as IDO1-AS6.4) located on the antisense-strand of IDO1 (Indoleamine-2,3 -dioxygenase 1, a tryptophan catabolizing enzyme), plays critical roles in the regulation of inflammation and tryptophan (Trp) catabolism. Our studies demonstrated that hLinfRNA7 expression is induced in human THP1-derived macrophages under inflammation (LPS or IFNγ- stimulation) and is localized in the nucleus. hLinfRNA7 knockdown suppressed LPS-induced IL-6, IL-1β, and iNOS expression and reduced nitric oxide production. Interestingly, hLinfRNA7 knockdown also downregulated the inflammation-induced expression of IDO1 as well as the tryptophan catabolite kynurenine level in macrophages, suggesting critical roles of hLinfRNA7 in inflammation, cytokine regulation, and Trp-catabolism. Furthermore, IDO1 also regulate hLinfRNA7 expression, suggesting their interplay in inflammation and Trp-catabolism. hLinfRNA7 also modulates NF-κB signaling and interacts with an RNA-binding protein, YBX1, which also regulates cytokines, IDO1, hLinfRNA7, and Trp-catabolism under inflammation. Our study demonstrates lncRNA hLinfRNA7 is a novel regulator of inflammation and tryptophan catabolism. By delineating an hLinfRNA7-YBX1-IDO1 axis, our study expands lncRNA roles in immune-metabolic control and inflammatory disease.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"855-886"},"PeriodicalIF":2.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13463789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148163775","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

Correction. 修正。

IF 2.7 2区生物学

Molecular and Cellular Biology Pub Date : 2025-11-14 DOI: 10.1080/10985549.2025.2578939

引用次数: 0

Expression of Concern: Mitogen Stimulation Cooperates with Telomere Shortening To Activate DNA Damage Responses and Senescence Signaling. 关注表达：丝裂原刺激与端粒缩短共同激活DNA损伤反应和衰老信号。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2025-02-24 DOI: 10.1080/10985549.2025.2462481

引用次数: 0

SIRT3 Deficiency Promotes Lung Endothelial Pyroptosis Through Impairing Mitophagy to Activate NLRP3 Inflammasome During Sepsis-Induced Acute Lung Injury. 在脓毒症诱导的急性肺损伤过程中，SIRT3缺陷通过损害有丝分裂来激活NLRP3炎症体，从而促进肺内皮细胞脓毒症。

IF 3.2 2区生物学

Molecular and Cellular Biology Pub Date : 2025-01-01 Epub Date: 2024-11-18 DOI: 10.1080/10985549.2024.2426282

Congmin Yan, Xin Lin, Jingting Guan, Wengang Ding, Ziyong Yue, Zhiqiang Tang, Xiangqi Meng, Bo Zhao, Zhiqiang Song, Dongmei Li, Tao Jiang

{"title":"SIRT3 Deficiency Promotes Lung Endothelial Pyroptosis Through Impairing Mitophagy to Activate NLRP3 Inflammasome During Sepsis-Induced Acute Lung Injury.","authors":"Congmin Yan, Xin Lin, Jingting Guan, Wengang Ding, Ziyong Yue, Zhiqiang Tang, Xiangqi Meng, Bo Zhao, Zhiqiang Song, Dongmei Li, Tao Jiang","doi":"10.1080/10985549.2024.2426282","DOIUrl":"10.1080/10985549.2024.2426282","url":null,"abstract":"Acute lung injury (ALI) is a major cause of death in bacterial sepsis due to endothelial inflammation and endothelial permeability defects. Mitochondrial dysfunction is recognized as a key mediator in the pathogenesis of sepsis-induced ALI. Sirtuin 3 (SIRT3) is a histone protein deacetylase involved in preservation of mitochondrial function, which has been demonstrated in our previous study. Here, we investigated the effects of SIRT3 deficiency on impaired mitophagy to promote lung endothelial cells (ECs) pyroptosis during sepsis-induced ALI. We found that 3-TYP aggravated sepsis-induced ALI with increased lung ECs pyroptosis and enhanced NLRP3 activation. Mitochondrial reactive oxygen species (mtROS) and extracellular mitochondrial DNA (mtDNA) released from damaged mitochondria could be exacerbated in SIRT3 deficiency, which further elicit NLRP3 inflammasome activation in lung ECs during sepsis-induced ALI. Furthermore, Knockdown of SIRT3 contributed to impaired mitophagy via downregulating Parkin, which resulted in mitochondrial dysfunction. Moreover, pharmacological inhibition NLRP3 or restoration of SIRT3 attenuates sepsis-induced ALI and sepsis severity in vivo. Taken together, our results demonstrated SIRT3 deficiency facilitated mtROS production and cytosolic release of mtDNA by impaired Parkin-dependent mitophagy, promoting to lung ECs pyroptosis through the NLRP3 inflammasome activation, which providing potential therapeutic targets for sepsis-induced ALI.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"1-16"},"PeriodicalIF":3.2,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647859","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

PARP1-Dependent and Independent Pathways for Resolution of Trapped Topoisomerase I Covalent Complexes. 捕获拓扑异构酶I共价复合物分解的parp1依赖和独立途径。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2025-01-01 Epub Date: 2025-09-16 DOI: 10.1080/10985549.2025.2555891

Benu Brata Das, Banhi Chowdhury, Sarita Das, Asmit Banerjee

{"title":"PARP1-Dependent and Independent Pathways for Resolution of Trapped Topoisomerase I Covalent Complexes.","authors":"Benu Brata Das, Banhi Chowdhury, Sarita Das, Asmit Banerjee","doi":"10.1080/10985549.2025.2555891","DOIUrl":"10.1080/10985549.2025.2555891","url":null,"abstract":"Topoisomerase I (Top1) alleviates DNA supercoiling during replication and transcription, but its catalytic cycle can be hijacked by chemotherapeutic agents such as camptothecin (CPT), stabilizing Top1-DNA covalent complexes (Top1cc) that threaten genome integrity. Efficient resolution of these trapped intermediates is crucial to prevent replication stress, DNA breaks, and cell death. Poly (ADP-ribose) polymerase 1 (PARP1) is a key sensor of Top1cc, facilitating repair by recruiting tyrosyl-DNA phosphodiesterase 1 (TDP1) and modifying chromatin to promote lesion accessibility. Beyond this canonical pathway, emerging evidence highlights PARP1-independent mechanisms such as endo nucleolytic cleavage, proteolytic degradation of Top1 and replication-associated processing. Intriguingly, PARP1 appears to act as a molecular switch between TDP1 and the endonuclease pathway for the repair of Top1cc. This review highlights mechanisms of PARP1-dependent and -independent Top1cc repair pathways, their interplay and redundancy, and how their targeting can enhance Top1-based cancer therapies and overcome resistance.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"603-622"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069991","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

Deciphering the m6A Epitranscriptomic Landscape of mRNAs in Breast Cancer Cells. 解读乳腺癌细胞中mrna的m6A表转录组学景观。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2025-01-01 Epub Date: 2025-10-06 DOI: 10.1080/10985549.2025.2560956

Konstantina Athanasopoulou, Panagiotis G Adamopoulos, Panagiotis Tsiakanikas, Glykeria N Daneva, Ioannis Prassas, George M Yousef, Eleftherios P Diamandis, Andreas Scorilas

{"title":"Deciphering the m6A Epitranscriptomic Landscape of mRNAs in Breast Cancer Cells.","authors":"Konstantina Athanasopoulou, Panagiotis G Adamopoulos, Panagiotis Tsiakanikas, Glykeria N Daneva, Ioannis Prassas, George M Yousef, Eleftherios P Diamandis, Andreas Scorilas","doi":"10.1080/10985549.2025.2560956","DOIUrl":"10.1080/10985549.2025.2560956","url":null,"abstract":"N6-methyladenosine (m6A), the most prevalent modification in mRNAs, influences mRNA stability, splicing, and translation. Dysregulation of m6A patterns has been linked to various diseases, including cancer, highlighting its significance in cellular homeostasis. However, accurate detection and precise quantification of m6A sites within individual transcripts remains challenging. In this study, we employed nanopore sequencing to achieve transcriptome-wide, base-resolution map of the m6A methylome in human breast cancer cells. By investigating m6A distribution across breast cancer cell lines and implementing a CRISPR/Cas9-based knockout of the major m6A eraser ALKBH5, we provide insights into the differential methylation levels and motif-specific characteristics of m6A transcriptomic sites. We elucidated the m6A epitranscriptome in five well-established breast cancer cell lines derived from distinct molecular subtypes of the disease and confirmed a DRACH-dependent activity of ALKBH5. Comparative methylation analysis with the non-cancerous MCF-10A cell line revealed that MCF-7 and BT-474 breast cancer cells are primarily hypomethylated, while BT-20, MDA-MB-231 and SK-BR-3 cells show widespread hypermethylation. These cell line-based patterns highlight the potential regulatory role of m6A in breast cancer heterogeneity. Overall, our findings enhance the understanding of m6A dynamics in breast cancer.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"660-679"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233033","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

Kinase Inhibitor-Induced Cell-Type Specific Vacuole Formation in the Absence of Canonical ATG5-Dependent Autophagy Initiation Pathway. 在缺乏典型atg5依赖性自噬起始途径的情况下，激酶抑制剂诱导细胞型特异性液泡形成。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2025-01-01 Epub Date: 2025-02-02 DOI: 10.1080/10985549.2025.2454421

Susan Jose, Himanshi Sharma, Janki Insan, Khushboo Sharma, Varun Arora, Sameera Puranapanda, Sonam Dhamija, Nabil Eid, Manoj B Menon

{"title":"Kinase Inhibitor-Induced Cell-Type Specific Vacuole Formation in the Absence of Canonical ATG5-Dependent Autophagy Initiation Pathway.","authors":"Susan Jose, Himanshi Sharma, Janki Insan, Khushboo Sharma, Varun Arora, Sameera Puranapanda, Sonam Dhamija, Nabil Eid, Manoj B Menon","doi":"10.1080/10985549.2025.2454421","DOIUrl":"10.1080/10985549.2025.2454421","url":null,"abstract":"Pyridinyl-imidazole class p38 MAPKα/β (MAPK14/MAPK11) inhibitors including SB202190 have been shown to induce cell-type specific defective autophagy resulting in micron-scale vacuole formation, cell death, and tumor suppression. We had earlier shown that this is an off-target effect of SB202190. Here we provide evidence that this vacuole formation is independent of ATG5-mediated canonical autophagosome initiation. While SB202190 interferes with autophagic flux in many cell lines parallel to vacuolation, autophagy-deficient DU-145 cells and CRISPR/Cas9 gene-edited ATG5-knockout A549 cells also undergo vacuolation upon SB202190 treatment. Late-endosomal GTPase RAB7 colocalizes with these compartments and RAB7 GTP-binding is essential for SB202190-induced vacuolation. A screen for modulators of SB202190-induced vacuolation revealed molecules including multi-kinase inhibitor sorafenib as inhibitors of vacuolation and sorafenib co-treatment enhanced cytotoxicity of SB202190. Moreover, VE-821, an ATR inhibitor was found to phenocopy the cell-type specific vacuolation response of SB202190. To identify the factors determining the cell-type specificity of vacuolation induced by SB-compounds and VE-821, we compared the transcriptomics data from vacuole-forming and non-vacuole-forming cancer cell lines and identified a gene expression signature that may define sensitivity of cells to these small-molecules. Further analyses using small molecule tools and the gene signature discovered here, could reveal novel mechanisms regulating this interesting anti-cancer phenotype.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"99-115"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080547","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

Hypoxia Signaling in the Cell Type-Specific Regulation of Erythropoietin Production Throughout Mammalian Development. 缺氧信号在哺乳动物发育过程中对促红细胞生成素产生的细胞类型特异性调节。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2025-01-01 Epub Date: 2025-06-27 DOI: 10.1080/10985549.2025.2522720

Norio Suzuki, Taku Nakai, Yuma Iwamura, Koichiro Kato

{"title":"Hypoxia Signaling in the Cell Type-Specific Regulation of Erythropoietin Production Throughout Mammalian Development.","authors":"Norio Suzuki, Taku Nakai, Yuma Iwamura, Koichiro Kato","doi":"10.1080/10985549.2025.2522720","DOIUrl":"10.1080/10985549.2025.2522720","url":null,"abstract":"To maintain the oxygen supply to peripheral organs, the production of erythropoietin (EPO), an essential growth factor for red blood cells, is controlled in a hypoxia-inducible manner in mammals. The developmentally earliest site of EPO production, which is necessary for primitive erythropoiesis in the yolk sac and bloodstream, is found in a subset of neural crest and neuroepithelial cells during mid-stage embryonic development. These neural EPO-producing (NEP) cells maintain their immaturity and EPO-producing ability in their hypoxic microenvironment, which is inherent in developing embryos. After oxygenation of the fetus by the establishment of the circulatory system and EPO-driven erythropoiesis, the site of EPO production shifts to hepatocytes of the fetal liver, where erythropoiesis also occurs. In adult mammals, a specific fibroblastic cell fraction in the renal interstitium, known as renal EPO-producing (REP) cells, secretes the majority of EPO to support bone marrow erythropoiesis. Hypoxia-inducible transcription factors (HIFs) are involved in EPO production across NEP cells, hepatocytes, and REP cells, whereas the regulatory mechanisms are distinct for each cell type. This review summarizes the molecular mechanisms of EPO gene regulation throughout all life stages and discusses the associations of HIF signaling in EPO production with other stimuli, including inflammation and metabolism.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"386-394"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144506558","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

Key Mechanisms in Lysosome Stability, Degradation and Repair. 溶酶体稳定性、降解和修复的关键机制。

IF 2.8 2区生物学

Molecular and Cellular Biology Pub Date : 2025-01-01 Epub Date: 2025-05-09 DOI: 10.1080/10985549.2025.2494762

Rui Zhang, Marc A Vooijs, Tom Gh Keulers

{"title":"Key Mechanisms in Lysosome Stability, Degradation and Repair.","authors":"Rui Zhang, Marc A Vooijs, Tom Gh Keulers","doi":"10.1080/10985549.2025.2494762","DOIUrl":"10.1080/10985549.2025.2494762","url":null,"abstract":"Lysosomes are organelles that play pivotal roles in macromolecule digestion, signal transduction, autophagy, and cellular homeostasis. Lysosome instability, including the inhibition of lysosomal intracellular activity and the leakage of their contents, is associated with various pathologies, including cancer, neurodegenerative diseases, inflammatory diseases and infections. These lysosomal-related pathologies highlight the significance of factors contributing to lysosomal dysfunction. The vulnerability of the lysosomal membrane and its components to internal and external stimuli make lysosomes particularly susceptible to damage. Cells are equipped with mechanisms to repair or degrade damaged lysosomes to prevent cell death. Understanding the factors influencing lysosome stabilization and damage repair is essential for developing effective therapeutic interventions for diseases. This review explores the factors affecting lysosome acidification, membrane integrity, and functional homeostasis and examines the underlying mechanisms of lysosomal damage repair. In addition, we summarize how various risk factors impact lysosomal activity and cell fate.","PeriodicalId":18658,"journal":{"name":"Molecular and Cellular Biology","volume":" ","pages":"212-224"},"PeriodicalIF":2.8,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12352500/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018298","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