Cells最新文献

{"title":"Unlocking the Role of Metabolic Pathways in Brain Metastatic Disease.","authors":"Madalena Pinto, Sara Violante, Rita Cascão, Claudia C Faria","doi":"10.3390/cells14100707","DOIUrl":"10.3390/cells14100707","url":null,"abstract":"<p><p>The dissemination of malignant cells to the brain is a late-stage complication of cancer, leading to significant morbidity and mortality. Brain metastases (BM) affect 20-30% of cancer patients, primarily originating from lung cancer, breast cancer, and melanoma. Despite advances in molecular-targeted therapies, brain metastatic disease remains incurable, with a poor median survival of ≤12 months if left untreated. The lack of therapeutic efficacy is mainly attributed to the presence of the blood-brain barrier (BBB) and genetic differences between BM and their primary tumors. Previously published data have identified potential driver mutations of BM. However, the mechanisms underlying brain cancer dissemination remain unknown. Recent studies emphasize the pivotal role of metabolic adaptations in supporting the metastatic process, particularly in the nutrient-poor microenvironment characteristic of the brain. Understanding the interplay between metabolism and genetic alterations associated with brain metastatic disease could unveil novel therapeutic targets that are more effective in treating patients. This review focuses on relevant metabolic pathways in cancer, particularly brain cancer dissemination, while also presenting information on current preclinical models of BM, relevant clinical trials, and preclinical studies targeting metabolic reprogramming, providing an overview for advancing therapeutic strategies in BM.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109720/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149313","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}

{"title":"Characterization of Extracellular Vesicles from Infrapatellar Fat Pad Mesenchymal Stem/Stromal Cells Expanded Using Regulatory-Compliant Media and Inflammatory/Hormonal Priming.","authors":"Marc Philippon, Ramy Labib, Michelle Bellas Romariz Gaudie Ley, Lee D Kaplan, Armando J Mendez, Thomas M Best, Dimitrios Kouroupis","doi":"10.3390/cells14100706","DOIUrl":"10.3390/cells14100706","url":null,"abstract":"<p><p>Osteoarthritis (OA) remains a leading cause of disability worldwide, with no disease-modifying therapies currently available for treatment. The infrapatellar fat pad (IFP) harbors mesenchymal stem/stromal cells (MSC) with potent immunomodulatory and regenerative properties, making them a promising candidate for OA treatment. A growing body of evidence suggests that the therapeutic effects of MSC are largely mediated by their extracellular vesicles (EVs), which carry bioactive cargo that modulates inflammation and tissue repair. However, optimizing MSC-derived EVs as a cell-free therapeutic approach requires an in-depth understanding of how culture conditions and inflammatory/hormonal priming influence their functional properties. In this study, IFP-MSC were expanded in regulatory-compliant human platelet lysate (HPL) and xeno-/serum-free (XFSF) media and primed with an inflammatory/fibrotic cocktail (TIC) with oxytocin (OXT) to assess the impact on their immunophenotypic profile and EV cargo. The immunophenotype confirmed that TIC+OXT-primed MSC retained key immunomodulatory surface markers, while EV characterization verified the successful isolation of CD63+/CD9+ vesicles. Pathway enrichment analysis of both HPL- and XFSF- TIC+OXT EVs cargo identified key miRNAs associated with immune regulation, tissue repair, and anabolic signaling. Functional assays revealed that TIC+OXT EVs promoted M2-like anti-inflammatory macrophage polarization and exhibited chondroprotective properties in chondrocytes/synoviocytes inflammatory osteoarthritic assay. These findings highlight the therapeutic potential of TIC+OXT-primed IFP-MSC-derived EVs as immunomodulatory and chondroprotective agents, offering a promising strategy for OA treatment through a clinically viable, cell-free approach.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149458","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}

{"title":"The Competitive Interaction of Alveolar Wall Distention with Elastin Crosslinking: A Mechanistic Approach to Emergent Phenomena in Pulmonary Emphysema.","authors":"Jerome Cantor","doi":"10.3390/cells14100702","DOIUrl":"10.3390/cells14100702","url":null,"abstract":"<p><p>Emergent phenomena arise from the interaction of competing forces at multiple scale levels, resulting in complex outcomes that are not readily apparent from analyzing the individual components. Regarding biological systems, when a critical threshold is reached, a phase transition occurs, producing a spontaneous system reorganization characterized by recognizable molecular, microscopic, and macroscopic changes. The current paper explores the emergent phenomena underlying the pathogenesis of pulmonary emphysema, a disease characterized by progressive airspace enlargement. The competitive relationship between mechanical strain imposed on alveolar walls and a countervailing increase in elastin crosslinking to prevent alveolar wall rupture leads to airspace enlargement as the balance between these two processes shifts toward increasing lung injury. This phase transition is also accompanied by an accelerated release of peptide-free elastin-specific desmosine crosslinks as the mean alveolar wall diameter begins to increase, suggesting their potential use as a biomarker for the molecular changes that precede the development of pulmonary emphysema. Early detection of the disease would allow more timely therapeutic intervention involving multiple agents that address the complexities of emergent phenomena at different scale levels.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110103/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149535","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}

{"title":"Aptamer-ODN Chimeras: Enabling Cell-Specific ODN Targeting Therapy.","authors":"Bei Xia, Qubo Zhu","doi":"10.3390/cells14100697","DOIUrl":"10.3390/cells14100697","url":null,"abstract":"<p><p>Oligonucleotides (ODNs) such as siRNA, saRNA, and miRNA regulate gene expression through a variety of molecular mechanisms and show unique potential in the treatment of genetic diseases and rare diseases, but their clinical application is still limited by the efficiency of the delivery system, especially the problem of the insufficient targeting of extrahepatic tissues. As homologous nucleic acid molecules, aptamers have become a key tool to improve the targeted delivery of ODNs. Aptamer-ODN chimeras can not only bind to multiple proteins on the cell surface with high specificity and selectivity, but they can also internalize into cells. Furthermore, they outperform traditional delivery systems in terms of cost-effectiveness and chemical modification flexibility. This review systematically summarizes the origin and progress of aptamer-ODN chimera therapy, discusses some innovative design strategies, and proposes views on the future direction of aptamer-ODN chimeras.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149454","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}

{"title":"Clinical Evidence of Mesenchymal Stromal Cells for Cerebral Palsy: Scoping Review with Meta-Analysis of Efficacy in Gross Motor Outcomes.","authors":"Madison C B Paton, Alexandra R Griffin, Remy Blatch-Williams, Annabel Webb, Frances Verter, Pedro S Couto, Alexey Bersenev, Russell C Dale, Himanshu Popat, Iona Novak, Megan Finch-Edmondson","doi":"10.3390/cells14100700","DOIUrl":"10.3390/cells14100700","url":null,"abstract":"<p><p>Mesenchymal stromal cells (MSCs) have been under clinical investigation for the treatment of cerebral palsy (CP) for over a decade. However, the field has been limited by study heterogeneity and variable reports of efficacy. We conducted a scoping review of published and registered reports of MSC treatment for CP, with meta-analysis of Gross Motor Function Measure (GMFM) outcomes to summarize research and provide future recommendations. Thirty published reports and 10 registered trials were identified, including 1292 people with CP receiving MSCs. Most received ≥2 doses (72%) of umbilical cord tissue MSCs (75%), intrathecally (40%) or intravenously (38%), and 31% were treated via compassionate/Expanded access. MSC treatment was safe and meta-analyses demonstrated that MSCs conferred significant improvements in GMFM at 3 - (1.05 (0.19-1.92), <i>p</i> = 0.02), 6 - (0.97 (0.30-1.64), <i>p</i> = 0.005) and 12 months (0.99 (0.30-1.67), <i>p</i> = 0.005) post-treatment. Whilst MSCs are safe and improve GMFM outcomes in CP with large effect sizes, study and participant variability continues to confound data interpretation and limits subgroup analyses. With no published Phase 3 trials and high rates of compassionate access, the field would benefit from well-designed trials with unified outcomes. Additionally, data sharing to enable Individual Participant Data Meta-Analysis would support the determination of optimal source, route and dose to progress towards regulatory approval.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110704/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149477","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}

{"title":"17β-Estradiol Promotes Tumorigenicity Through an Autocrine AREG/EGFR Loop in ER-α-Positive Breast Cancer Cells.","authors":"Sun Young Yoon, Yisun Jeong, Jai Min Ryu, Se Kyung Lee, Byung Joo Chae, Jonghan Yu, Seok Won Kim, Seok Jin Nam, Sangmin Kim, Jeong Eon Lee","doi":"10.3390/cells14100703","DOIUrl":"10.3390/cells14100703","url":null,"abstract":"<p><p>We previously reported that the level of EGFR expression is directly associated with the survival rate of estrogen receptor-positive (ER+) breast cancer patients. Here, we investigated how ER activation by 17β-estradiol (E2), the most potent form of estrogen, affects the expression or activity of EGFR or EGFR-related genes in ER+ breast cancer cells. As expected, E2 enhanced cell proliferation, the induction of S phase, and tumor growth in ER+ breast cancer models. E2 also increased the expression of secretory proteins, including amphiregulin (AREG), angiogenin, artemin, and CXCL16. We focused on AREG, which is a ligand of the epidermal growth factor receptor (EGFR). The levels of AREG expression were positively correlated with ESR1 expression. Our results also showed higher AREG mRNA expression levels in ER+ breast cancer cells than in ER- breast cancer cells. We treated ER+ breast cancer cells with lapatinib to inhibit the AREG/EGFR signaling pathway and then completely inhibited E2-induced cell proliferation and S-phase induction. Similar to the lapatinib treatment, cell proliferation, S-phase induction, cell migration, and tumor growth were suppressed by AREG knockdown. Taken together, we demonstrated that the induction of AREG by E2 contributes to EGFR activation, which then affects cell proliferation and tumor growth. Therefore, we suggest that AREG acts as an intermediary between EGFR and ER and targeting both ERs and EGFRs through combination therapy could prevent tumor progression in EGFR+ ER+ breast cancer patients.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149367","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}

{"title":"Dux Is Dispensable for Skeletal Muscle Regeneration: A Study Inspired by a \"Red Flagged\" Publication and Editorial Oversight.","authors":"Kenric Chen, Erdong Wei, Ana Mitanoska, Micah D Gearhart, Michael Kyba, Darko Bosnakovski","doi":"10.3390/cells14100695","DOIUrl":"10.3390/cells14100695","url":null,"abstract":"<p><p>Double homeobox (DUX) genes are key embryonic regulators that are silenced after the early cleavage stages of embryogenesis. Aberrant expression of DUX4 in skeletal muscle is linked to facioscapulohumeral muscular dystrophy (FSHD). A recent study reported that Dux, the murine ortholog of DUX4, contributes to the dystrophic phenotype in mdx mice, a Duchenne muscular dystrophy (DMD) model, and that its deletion enhances muscle regeneration by reducing oxidative stress. However, convincing evidence of Dux expression in either intact or injured muscle of wild-type (WT) and mdx mice remains lacking, raising questions about its role in muscle homeostasis. To investigate this, we assessed Dux expression in WT and mdx mice and used <i>Dux</i> knockout (Dux^Δ/Δ) mice to evaluate its function during regeneration following cardiotoxin (CTX)-induced injury. Contrary to prior reports, Dux was not expressed in either WT or mdx mice. Moreover, Dux deletion did not enhance muscle regeneration or affect the expression of the oxidative stress regulator Nrf2 following CTX injury. Lastly, we confirmed that neither DUX4 nor its target genes were induced in muscle biopsies from DMD patients, excluding a role for DUX4 in DMD pathology. Collectively, our results demonstrate that Dux does not impact skeletal muscle regeneration or DUX4 contribution to the DMD dystrophic phenotype, directly challenging the conclusions of a previously published study. We comment on issues of editorial oversight that led to the publication of that study and highlight the deleterious impact of the growing wave of fraudulent publications.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144148946","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}

{"title":"Non-Redundant Essential Roles of Proteasomal Ubiquitin Receptors Rpn10 and Rpn13 in Germ Cell Formation and Fertility.","authors":"Wan-Yu Yue, Yi Zhang, Tian-Xia Jiang, Xiao-Bo Qiu","doi":"10.3390/cells14100696","DOIUrl":"10.3390/cells14100696","url":null,"abstract":"<p><p>Primordial germ cells (PGCs) undergo proliferation, migration, and sexual differentiation to produce gonocytes, which eventually generate germ cells. The proteasome, which degrades most cellular proteins, is a protein complex with dozens of subunits. The proteasomal ubiquitin receptors Rpn10 and Rpn13 have been shown to play partially overlapping roles in binding ubiquitin chains in vitro and in liver function in vivo. However, the specific role of Rpn10 and Rpn13 in germ cell production remains unclear. We show here that Rpn10 and Rpn13 are each essential for germ cell production and fertility. The conditional deletion of either Rpn10 or Rpn13 in PGCs results in infertility in both male and female mice. Germ cells in testes and ovaries all decreased dramatically in the Rpn13 conditional knockout (<i>cKO</i>) mice. Specifically, the deletion of Rpn13 in PGCs disrupts the assembly of the 26S proteasome, reduces the number of PGCs, and blocks the meiosis of spermatocytes at the zygotene stage during prophase I; on the other hand, the deletion of Rpn10 in PGCs sharply reduces PGC migration. These results are important for understanding the roles of Rpn10 and Rpn13 in germ cell development and related reproductive diseases.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12110300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149486","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}

{"title":"Dauricine Impedes the Tumorigenesis of Lung Adenocarcinoma by Regulating Nrf2 and Reactive Oxygen Species.","authors":"Waleed Yousuf, Nimra Zafar Siddiqui, Perbhat Ali, Shaoxuan Cheng, Immad Ansari, Jialiang Song, Minghe Dai, Zhiyuan Qiu, Yue Zhu, Yaowen Zhang, Shuyan Liu, Yingqiu Zhang, Zhenhua Liu, Han Liu","doi":"10.3390/cells14100698","DOIUrl":"10.3390/cells14100698","url":null,"abstract":"<p><p>Dauricine has been shown to possess intriguing anti-cancerous activities against various malignancies. The current study examined the inhibitory effects of dauricine against lung adenocarcinoma with cell lines and animal models. MTT assay was performed in three different lung adenocarcinoma cell lines using a concentration range of dauricine. Colony formation, wound healing, Edu incorporation, and cell cycle analysis were conducted to investigate the impact of dauricine on lung adenocarcinoma cells in vitro. Moreover, flow cytometry was performed to observe the effect of dauricine on cellular ROS levels. The expression of redox regulator Nrf2 and apoptosis-related markers was assessed by Western blot. Importantly, the anti-tumor efficacy of dauricine was studied in vivo with two lung adenocarcinoma animal models, including a subcutaneous cell line-derived syngeneic model and an inducible orthotopic <i>KRAS^G12D</i>-driven lung adenocarcinoma model. The proliferation and migration of lung adenocarcinoma cells were significantly reduced by dauricine treatment. Flow cytometry analysis revealed that dauricine treatment resulted in cell cycle arrest at G0/G1 phases in A549, H1299, and A427 cells. Intracellular ROS levels were markedly augmented by dauricine treatment. Notably, dauricine led to the downregulation of the master redox regulator Nrf2. Meanwhile, dauricine treatment resulted in decreased Bcl-2 levels but elevated expression of BAX and cleaved Caspase 3. Finally, dauricine demonstrated significant efficacy in restricting tumor progression in both subcutaneous syngeneic and orthotopic lung adenocarcinoma models. Our results corroborate the anti-cancer effects of dauricine against lung adenocarcinoma with in vivo and in vitro analyses. Our findings also provide mechanistic evidence that links the impact of dauricine to cell cycle blockage and ROS-mediated apoptosis.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149496","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}

{"title":"Use of Tissue Specimens from Stereotactic Biopsies for Patient-Derived GBM Organoid-Based Drug Testing.","authors":"Amélie Wöllner, Adrian Paul, Maddalena Arquilla, Junguo Cao, Catharina Lotsch, Gerhard Jungwirth, Lena Jassowicz, Andreas von Deimling, Andreas W Unterberg, Sandro M Krieg, Martin Jakobs, Rolf Warta, Christel Herold-Mende","doi":"10.3390/cells14100701","DOIUrl":"10.3390/cells14100701","url":null,"abstract":"<p><p><i>IDH</i>-wildtype glioblastoma (GBM) represents the most common malignant form of brain tumor and is still incurable despite comprehensive therapeutic efforts. Due to tumor location and patient condition, open surgical resection of recurrent GBM is not always feasible. In these cases, frame-based stereotactic biopsies represent a less invasive technique to obtain tissue samples for diagnostics. However, whether this material would also be sufficient to prepare tumor organoids (TOs) and perform drug screenings has not been addressed so far. In this study, we present our highly optimized workflow for generating standardized patient-derived GBM TOs from single-cell suspensions using limited biopsy-derived material. We highlight crucial steps within the procedure, such as reliable cell counting, viable cell recovery, enzymatic digestion, and the requirement of an extracellular matrix as a scaffold. Furthermore, we showcase the potential of personalized drug testing as a promising application of GBM TOs. In conclusion, we successfully developed a robust workflow that effectively utilizes the limited material derived from stereotactic biopsies to reproducibly form standardized TOs. Moreover, we demonstrate that biopsy-derived TOs represent a valuable tool for testing drug vulnerabilities in a personalized setting, which might be especially useful in the case of non-resectable GBM.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 10","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12109714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144149343","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}