Bioscience Reports最新文献

{"title":"Targeting the MYCN interaction network in neuroblastoma.","authors":"Chelsea Xinyi Yow, Sharon Yeoh, Eoin Leen, Richard Bayliss","doi":"10.1042/BSR20250104","DOIUrl":"10.1042/BSR20250104","url":null,"abstract":"<p><p>Neuroblastoma is a common solid tumour in children and accounts for a disproportionate share of childhood cancer mortality. High-risk neuroblastoma is a major clinical challenge, with survival rates below 50% despite intensive therapy. Amplification of the MYCN oncogene is a hallmark of high-risk disease. MYCN protein is a transcription factor that promotes proliferation and blocks differentiation. MYCN is often described as 'undruggable' due to its lack of enzymatic activity and intrinsically disordered nature that means it lacks well-defined binding pockets for small molecules. This review explores the molecular interactome of MYCN as an opportunity for therapeutic discovery. We highlight functional and structural features of the interactions with key partners, such as MAX, WDR5, TFIIIC5 and Aurora kinase A. We discuss emerging strategies to disrupt MYCN interactions and to enable its degradation through disruption of protein stabilisation mechanisms or the use of degraders such as proteolysis targeting chimeras. By integrating knowledge of MYCN biology, molecular structures and chemical biology, these approaches provide promising routes towards targeted therapies for MYCN-driven neuroblastoma.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13270163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148219","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum-free culture with PVP enables maintenance of primary culture of parathyroid cells in vitro.","authors":"Natsumi Iwawaki, Toshiyuki Takehara, Atsuhiro Tatemizo, Takeshi Teramura","doi":"10.1042/BSR20253933","DOIUrl":"10.1042/BSR20253933","url":null,"abstract":"<p><p>The parathyroid gland is a critical endocrine organ responsible for maintaining serum calcium homeostasis through the secretion of parathyroid hormone (Pth). Parathyroid tissue can be irreversibly lost due to autoimmune diseases or surgical injury, and the absence of appropriate model cells has hindered drug discovery targeting this cell type. Therefore, there is a strong need to develop in vitro culture systems for normal parathyroid cells for both cell therapy and pharmacological research. In the present study, we identified a serum-free culture system supplemented with B27 and polyvinylpyrrolidone that enables the maintenance of parathyroid-like cells. These cells retained expression of key markers such as calcium-sensing receptor and Pth and exhibited slow but consistent colony formation and proliferation. Notably, the cultured cells were highly sensitive to serum exposure; the addition of 10% fetal bovine serum rapidly induced epithelial-to-mesenchymal transition-like changes and a marked loss of functional gene expression. These findings not only provide a foundational strategy for culturing parathyroid cells but also highlight their inherent vulnerability to phenotypic and functional deterioration.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of vitamin B1/B6/B12 supplementation with sphingosine-1-phosphate signaling and its receptors in multiple sclerosis patients: relevance to LISPR1 and APOA1-AS.","authors":"Noha A Mehana, Heba R Ghaiad, Mohammed M Nooh, Mai A Amer, Lobna Talaat El-Ghoneimy, Maheera H Safwat","doi":"10.1042/BSR20260065","DOIUrl":"10.1042/BSR20260065","url":null,"abstract":"<p><p>MS is a lifelong autoimmune disorder striking the central nervous system (CNS). Despite the currently used disease-modifying therapies, patients are exposed to persistent neuropathy, pinpointing the need for supportive therapy. Neurotropic vitamins B1, B6, and B12 have been used to offer relief from immunological and neurological MS manifestations. The present study aimed to provide some mechanistic insights into the relationship of B1/B6/B12 vitamin supplementation with the development of MS regarding lipid metabolism and epigenetics. In this cross-sectional observational study, blood samples were obtained from 53 MS patients, including 25 patients, who had received daily vitamin B1/B6/B12 supplementation for over six months and 28 patients without supplementation. Plasma sphingosine-1-phosphate (S1P) and S1P receptor-1 (S1PR1) levels, lipid profile, and gene expression of ApoA1, sphingosine kinases 1&2 (SPHK1&2), S1PR1, as well as the lncRNAs APOA1-AS and LISPR1 were evaluated. Gene ontology and KEGG pathway enrichment analyses were conducted. Vitamin B1/B6/B12 supplementation was associated with a more favorable lipid profile. Supplemented patients also exhibited higher ApoA1 and lower APOA1-AS expressions compared with non-supplemented patients. Additionally, vitamin B1/B6/B12 supplementation was associated with lower expression levels of SPHK1, SPHK2, LISPR1, and S1PR1 and reduced circulating S1P concentrations. These findings imply significant associations between long-term vitamin B1/B6/B12 supplementation and alterations in lipid-related markers and sphingosine-associated signaling in MS patients. However, the observational design, selection bias, and small sample size limit causal inference and may not fully capture the heterogeneity of MS population. Besides, supplement adherence was self-reported and not objectively verified, and circulating vitamin levels were not measured.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13199797/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Shaoyao-Gancao Decoction alleviated hyperandrogenism in a letrozole-induced rat model of polycystic ovary syndrome by inhibition of NF-κB activation.","authors":"Jun-Jin Liu, Rui-Gang Hou, Yun-Yun Shao, Zhuang-Peng Chang, Yao Cheng, Xin-Chun Wang, Jing-Ping Zhang, Xiao-Juan Feng, Yi-Ting Guo","doi":"10.1042/BSR20181877_RET","DOIUrl":"10.1042/BSR20181877_RET","url":null,"abstract":"","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13258057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148148228","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apolipoprotein variations across APOE genotypes in young and elderly patients with coronary heart disease.","authors":"Yuxuan Zhang, Siwei Li, Shijie Xu, Rui Zhao, Fang Zheng, Junfang Wu","doi":"10.1042/BSR20260258","DOIUrl":"10.1042/BSR20260258","url":null,"abstract":"<p><p>Both the Apolipoprotein E (ApoE) genotype and apolipoprotein (Apo) profiling are closely associated with the risk of coronary heart disease (CHD). However, it remains unclear whether APOE genotypes modulate the distribution of Apos and whether such regulation differs between young and elderly CHD patients. The present study aims to investigate the effects of APOE genotypes on the levels of plasma Apos in both young and elderly CHD patients. Two datasets were analyzed. Dataset 1 included 293 CHD patients with APOE genotyping. The quantification of 4 APOE isoform-specific peptides and 16 Apos was simultaneously measured in plasma using liquid chromatography-mass spectrometry. Dataset 2 comprised 3821 CHD participants from UK Biobank, for whom Apo levels were obtained through Olink proteomics. Selected Apos identified in dataset 1 were independently validated in dataset 2. We developed a robust method for simultaneous quantification of APOE isoforms and Apos in human plasma. APOE genotype results from liquid chromatography-mass spectrometry were fully consistent with those from the TaqMan assay in all patients. Among the measured Apos, the levels of ApoL1 were significantly decreased in elderly CHD patients, which were independently validated in the UK Biobank cohort, particularly in those carrying APOΕ ε3 and ε4 alleles. Mediation analysis revealed that ApoL1 statistically mediated the association between age and CHD status. Our results suggested that APOE polymorphisms affect the plasma Apo profiles and that ApoL1 is associated with older CHD patients carrying the APOE ε3 and ε4 genotypes.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13270160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148040437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid metabolism as a marker for glioma aggressiveness.","authors":"Hennrique Taborda Ribas, Guilherme Taborda Ribas, Arquimedes Paixão de Santana-Filho, Ana Gabriela Jungles, Clementina Mesaros, Dieval Guizelini, Glaucia R Martinez, Marina Trombetta-Lima, Guilherme Lanzi Sassaki, Sheila M B Winnischofer","doi":"10.1042/BSR20253270","DOIUrl":"10.1042/BSR20253270","url":null,"abstract":"<p><p>Glioblastoma (GBM) is the most aggressive type of central nervous system tumor. There have been advances in glioma biology understanding; however, the current therapies are still inefficient. Additionally, new molecular markers are being explored for glioma grading, offering potential for novel diagnostic and drug targets. Considering the important role of lipid metabolism in tumorigenesis, understanding the lipid-related pathways in glioma could lead to new important markers. Here, lipid metabolism was analyzed by integrating two different data sources, the transcriptome data from The Cancer Genome Atlas and experimental data from tumor cells, to investigate how lipid metabolism is regulated in glioma. We compared the expression of 743 lipid-related genes in public RNAseq data of glioma patients (n = 681) to lipidomic analyses of glioblastoma cell lines (A172, U87MG, and T98G). We identified 29 lipid-related genes correlated to prognosis and constructed a risk signature based on these genes. Extracellular matrix-related genes were positively correlated to the risk score. Our findings revealed that aggressiveness is linked to alterations in membrane composition, characterized by an increase in phospholipids, coupled with a decrease in cholesterol and fatty acid unsaturation levels, which impact membrane physical properties. Modulation of critical signaling lipids, specifically sphingolipids, was also observed. Here, we identify lipid markers that may play a significant role in glioma. The converging axis involving sphingomyelinase and sphingosine-1-phosphate, mediated by the actions of sphingomyelinase SMPD1 and sphingosine-kinase SPHK1, emerged as a pivotal factor in glioma. The present study suggests that lipid membrane composition is pivotal for the GBM aggressiveness.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13234697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147961960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rewiring mTOR signaling in Alzheimer's disease: emerging mTOR modulators beyond oncology.","authors":"Benedikt Jakob Lohnes, Aneta Myskova, Arti Tyagi, Udo Frank Hartwig, Nitesh Kumar Poddar","doi":"10.1042/BSR20260203","DOIUrl":"10.1042/BSR20260203","url":null,"abstract":"<p><p>While Alzheimer's disease (AD) is the most common cause of dementia, curative treatments remain unavailable. Despite distinct pathologies between AD and cancer, shared dysregulation of the PI3K-AKT-mTOR signaling pathway promotes both disease states. mTOR activity significantly contributes to AD hallmarks, including amyloid-beta production, tau hyperphosphorylation, and altered metabolism and autophagy through mTOR-mediated signaling and downstream targets such as BACE-1, GSK-3β, and AChE. Consequently, mTOR-modulating compounds, demonstrating promising results in oncology, present a viable strategy to potentially halt or reverse AD progression. This review discusses the potential application of 37 mTOR pathway-modulating compounds, many originally developed for cancer treatment, given their shared molecular targets. We systematically classified the compounds based on their origin as marine, plant-derived, structural analogs, and synthetic compounds. This framework reveals a fundamental trade-off, as the structural novelty and pleiotropic effects of natural products are often counterbalanced by poor pharmacokinetics, whereas the pharmacological precision of synthetic compounds is frequently limited by compensatory feedback loops. Furthermore, we analyze translational challenges, including balancing efficacy with toxicity, limitations in blood-brain barrier penetration, and the need for patient stratification using robust biomarkers. We conclude that the most promising therapeutic approach for AD involves synergistically combining natural products with rational synthetic design. Leveraging natural products as a source of novel chemical scaffolds and employing targeted synthetic engineering to overcome their pharmacokinetic limitations, this strategy moves beyond blunt pathway inhibition. Ultimately, this enables a highly nuanced modulation of the mTOR network, providing the basis for future preclinical and clinical drug development in AD.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13259829/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148210029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aerobic exercise is associated with divergent regulation of macrophage migration inhibitory factor and enhanced remyelination in experimental autoimmune neuritis.","authors":"Yantong Liu, Xiaohan Shi, Ying Wang, Yunhao Deng, Haoyue Chen, Hao Zhang, Yuwen Hao, Ling Zheng, Xiaoyu Wang, Zuncheng Zheng, Kai Wang, Xiaojing Yuan","doi":"10.1042/BSR20260227","DOIUrl":"10.1042/BSR20260227","url":null,"abstract":"<p><p>The present study investigated the association between aerobic exercise preconditioning and macrophage migration inhibitory factor (MIF) expression, as well as myelination in the sciatic nerve in experimental autoimmune neuritis (EAN) rats. Female Lewis rats underwent 4-week swimming protocols including high-intensity daily, moderate-intensity daily, and moderate-intensity alternate-day (MOD-AltDay) regimens prior to EAN induction, with control groups of EAN without exercise and Sham operation. Assessment of disease severity, nerve conduction velocity, and sciatic nerve pathology revealed that the moderate-intensity alternate-day exercise regimen significantly delayed disease onset, lowered peak clinical scores, and improved neurological function. Molecular analyses demonstrated that this protective effect was mediated through divergent regulation of MIF: systemic MIF was substantially suppressed (27205.94 ± 4291.76 pg/ml versus EAN 71075.61 ± 10166.41 pg/ml; P <0.001) with concomitant reduction in macrophage infiltration, while local MIF expression within the sciatic nerve was significantly elevated (P <0.01), correlating with enhanced remyelination as evidenced by increased myelin sheath area (LFB: 67.42 ± 3.26% versus EAN 40.64 ± 9.63%, P <0.01) and elevated myelin basic protein expression (0.92 ± 0.14 AU versus EAN 0.59 ± 0.02 AU, P <0.05). Crucially, both high-intensity daily and moderate-intensity daily exercise protocols failed to confer comparable benefits. These findings indicate that the protective effect of MOD-AltDay exercise preconditioning on EAN is associated with tissue-specific regulation of MIF, and this change correlates with reduced systemic inflammation and enhanced local remyelination. Pharmacological/genetic studies are needed to confirm mechanisms and evaluate this exercise regimen as a non-pharmacological intervention for autoimmune neuropathy.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13223392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive overview of the biological foundations of ADHD.","authors":"Isabella Folego-Temoteo, Yago C Lima, Eugenio H Grevet, Marcos V Vidor, Maria Eduarda de A Tavares, Bruna S da Silva, Claiton H D Bau, Diego L Rovaris","doi":"10.1042/BSR20254061","DOIUrl":"10.1042/BSR20254061","url":null,"abstract":"<p><p>Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental condition marked by persistent and impairing patterns of inattention, hyperactivity, and impulsivity. Evidence from neurochemical, pharmacological, and genetic research supports the hypothesis that ADHD involves alterations in neurotransmission, primarily within dopaminergic and noradrenergic systems, with contributions from other neurotransmitter pathways and their interactions. Neuroimaging studies identify structural and functional differences in regions such as the frontal cortex and subcortical structures, although findings remain heterogeneous. Genomic research indicates a polygenic basis, with common and rare variants influencing synaptic transmission, neuronal development, regulatory pathways, and related biological processes. These studies also point to shared genetic influences between ADHD and psychological, social, and somatic traits. Additional omics approaches have further expanded these insights, although larger and more integrative studies across multiple layers remain needed. Environmental factors not only influence the onset of ADHD but also shape its course and prognosis, with emerging evidence highlighting complex gene-environment correlations and interactions. Together, the heterogeneity of findings across neuroimaging, genomic, and multi-omics studies underscores the importance of integrative approaches that embrace diversity across populations, methodologies, and biological systems. The present review provides a comprehensive overview of ADHD's biological foundations, highlighting central nervous system mechanisms, their interplay with genetic and environmental factors, and recent advances from multi-omics research with translational potential. We also discuss key methodological considerations, emphasizing that the biological architecture of ADHD is complex, highly polygenic, and spans multiple levels of analysis.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 6","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13259830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148210070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tubulogenesis of bovine uterine glands by epidermal growth factor and collagen I in 3D culture systems.","authors":"Yosuke Sugino, Rei Ichikawa, Shuichi Matsuyama, Yuki Yamamoto, Kohei Kawano, Koji Kimura","doi":"10.1042/BSR20260010","DOIUrl":"10.1042/BSR20260010","url":null,"abstract":"<p><p>Uterine glands are endometrial exocrine epithelia that support early embryo development. Their secretions are particularly essential for conceptus elongation in cattle. Uterine glands develop from the luminal epithelium and elongate into the stromal layer toward the myometrium. This process is regulated by growth factors, WNT proteins, and the surrounding extracellular matrix (ECM); however, the precise mechanisms that govern bovine uterine gland morphogenesis remain unclear. In this study, we determined how these signaling factors and ECM components affect the tubular formation of bovine uterine gland fragments in 3D culture systems. Uterine gland fragments were enzymatically isolated from bovine endometria and 3D-cultured in Matrigel with or without growth factors (EGF, FGF1, FGF2, FGF7, FGF10, and IGF-1) and WNT (WNT3A, WNT5A, and WNT7A) proteins. Of these, only EGF stimulated the elongation of uterine gland fragments and eventually induced the formation of uterine gland-like structures. EGF-induced tubulogenesis was accompanied by a rapid increase in cell proliferation and alterations in cell-ECM interactions. The supplementation of collagen I with Matrigel further promoted the elongation of the tubular structures. Although the addition of collagen I did not alter the gene expression profiles of the uterine gland-like structures, the integrin-ROCK pathway contributed to the collagen-induced enhancement of elongation. Our findings clarified that EGF and collagen I, but not FGFs, IGF-1, or WNTs, are key regulators for the tubular formation of 3D-cultured bovine uterine gland fragments. This 3D culture system provides a new platform to examine the cellular and molecular mechanisms underlying bovine uterine gland morphogenesis.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.5,"publicationDate":"2026-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13259824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147637871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}