{"title":"VHL Suppresses Angiogenesis Through HIF-1a-Mediated Ang/Tie2/AMPK/VEGF Signaling Pathway in Tie-2 Expressed Macrophages (TEMs).","authors":"Min-Cheng Zou, Yu-Hao Yang, Yun-Peng Mao, Ya Liu, Hui-Bing Gao, Wen-Dong Liu, Jia Liu, Fu-Yong Zhang","doi":"10.1007/s10528-025-11175-3","DOIUrl":"https://doi.org/10.1007/s10528-025-11175-3","url":null,"abstract":"<p><p>The cartilage of the growth plate is crucial for the longitudinal growth of long bones but is highly susceptible to injury due to its avascular nature. Growth plate injuries frequently result in the formation of a bone bridge, leading to limb length discrepancies and angular deformities. Angiogenesis is a critical factor in the repair process, as new blood vessels deliver oxygen, nutrients, and cellular components essential for bone regeneration. Tie2-expressing macrophages (TEMs) play a pivotal role in promoting angiogenesis in tumors and remodeled tissues; however, their precise function and regulatory mechanisms in epiphyseal plate injury repair remain unclear. This study investigates the role of the VHL/HIF-1α/Tie2/AMPK/Autophagy axis in TEM-mediated angiogenesis. Our findings identify VHL as a key regulator of TEM-driven angiogenesis, where VHL overexpression suppresses, and VHL silencing enhances the pro-angiogenic potential of TEMs. Mechanistically, VHL downregulates HIF-1α, reducing Tie2 surface expression, which in turn modulates AMPK-mediated autophagy. This pathway influences VEGF secretion, thereby promoting endothelial cell proliferation, migration, survival, and tube formation. These findings uncover a novel regulatory mechanism governing TEM-mediated angiogenesis and offer insights into potential therapeutic strategies to enhance vascularization, improve growth plate injury repair, and mitigate long-term orthopedic complications.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648161","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}
{"title":"EGCG Alleviates Lipopolysaccharide-Induced Septic Shock by Inhibiting NET-Mediated ROS Production by Regulating CXCL2 Expression.","authors":"Xiao Wang, Fantuo Kong, Qian Liu, Xiaoting Liu","doi":"10.1007/s10528-025-11198-w","DOIUrl":"https://doi.org/10.1007/s10528-025-11198-w","url":null,"abstract":"<p><p>In septic shock, neutrophil extracellular traps (NETs)-mediated reactive oxygen species (ROS) drive inflammation and organ failure, with reducing excessive NETs emerging as a therapeutic strategy. This study aimed to investigate whether chemokine (C-X-C motif) ligand 2 (CXCL2), previously linked to NET formation in acute lung injury (ALI), serves as a target for septic shock and whether epigallocatechin-3-gallate (EGCG) exerts protective effects via CXCL2. Through bioinformatics analysis and RT-qPCR, CXCL2 was found highly expressed in serum from septic shock patients and lipopolysaccharide (LPS)-induced septic rats, correlating with increased NETs (MPO-DNA, dsDNA, and H3Cit) and pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). In vitro, knocking down CXCL2 in human neutrophils significantly inhibited phorbol myristate acetate (PMA)-induced NETs formation and ROS production. In septic rats, treatment with EGCG reduced the levels of CXCL2 in serum and bronchoalveolar lavage fluid (BALF), suppressed markers of NETs in serum, BALF, and lung tissue, and alleviated lung inflammation. In vitro, EGCG significantly inhibited PMA-induced NETs formation and ROS production. Mechanistically, EGCG inhibited NETs and ROS by downregulating CXCL2, with these effects reversed by the overexpression of CXCL2. These findings confirm that CXCL2 promotes NET-mediated ROS production in septic shock, and EGCG alleviates injury by targeting CXCL2, highlighting CXCL2 as a potential therapeutic target and EGCG as a promising agent for septic shock treatment.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648160","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}
Junshen Xiao, Xu Cheng, Dou Huang, Shichao Wei, Zhaoyang Hu
{"title":"Functions of the KCNE Gene Family in Ion Channels.","authors":"Junshen Xiao, Xu Cheng, Dou Huang, Shichao Wei, Zhaoyang Hu","doi":"10.1007/s10528-025-11202-3","DOIUrl":"https://doi.org/10.1007/s10528-025-11202-3","url":null,"abstract":"<p><p>The KCNE gene family is crucial for physiological and pathological processes in the body and encodes small transmembrane proteins that function as auxiliary subunits to regulate voltage-gated potassium channels (K<sub>v</sub> channels). This family includes five members, KCNE1, KCNE2, KCNE3, KCNE4, and KCNE5, whose encoded proteins are referred to as MinK and MinK-related peptides (MiRPs), which influence the properties and localization of K<sub>v</sub>. When KCNE is coexpressed with Kv, it can alter the conductance, gating kinetics, and pharmacology of the channel. Therefore, these genes are particularly important for action potentials in excitable cells, and mutations in these genes can lead to significant diseases. In this paper, we review the functional roles of KCNE genes and their effects on Kv α subunits to further understand the regulatory effects of KCNE in modulating ion channels.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641424","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}
Gabriella Guo Sciriha, Josef Borg, Janet Sultana, Joseph Borg
{"title":"Transcriptome Analysis of TGFBI Knockdown vs Normal Corneal Epithelial Cells: Implications for TGFBI Corneal Dystrophy Treatment.","authors":"Gabriella Guo Sciriha, Josef Borg, Janet Sultana, Joseph Borg","doi":"10.1007/s10528-025-11191-3","DOIUrl":"https://doi.org/10.1007/s10528-025-11191-3","url":null,"abstract":"<p><p>This study aimed to clarify the role Transforming Growth Factor Beta Induced (TGFBI) protein plays in corneal epithelial homeostasis by using RNA interference and to explore the possibility of gene therapy as a treatment modality for the visually debilitating TGFBI Corneal Dystrophies (CDs). TGFBI knockdown (KD) in Human Corneal Epithelial Cells (HCECs) was performed by using shRNA lentiviral vectors. RNA sequencing and comprehensive transcriptome analysis were performed to investigate the differential expression between control HCECs and TGFBI KD HCECs. Over Representation Analysis of the differentially expressed (DE) genes delineated the effect inhibition of TGFBI would have on molecular pathways, corneal structure and function. An effective KD of 70.5% was achieved. The functions of downregulated genes in TGFBI KD HCECs indicate decreased inflammation (MTPN, IL1B, IL6, JAK2), decreased angiogenesis (CD24, IL6, JAK2), and decreased corneal scarring (AREG, ITGA11). The functions of upregulated genes indicate increased ECM remodeling, fibrosis, and neovascularisation (MMP2, AKT1, COL6A1, COL6A2), increased integrin signaling (ICAM, ITGA6), and increased cell proliferation (AKT1, ITGA6). Enriched associations of the DE genes included cell adhesion molecules, ECM structural constituents, RNA transport & metabolism, SMAD2/SMAD3:SMAD4 modulation, JAK-STAT and PI3K-Akt signaling pathways. This proof-of-concept study shows that it is possible to effectively silence TGFBI with shRNA in HCECs and provides valuable insight into how TGFBI dysfunction might impact corneal epithelial function. In view of the lack of targeted treatment available, the therapeutic potential of shRNA targeting TGFBI should be explored further since it can potentially revolutionize the future management of TGFBI CDs.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641425","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}
{"title":"The Clinical Value of hsa_circ_0000419 in Diagnosis and Prognosis of Esophageal Squamous Cell Carcinoma.","authors":"Yuanmei Dong, Huiling Meng, Yijia Chen, Huiwen Guo, Xiaoming Shi, Qibin He, Dongliang Mao","doi":"10.1007/s10528-025-11194-0","DOIUrl":"https://doi.org/10.1007/s10528-025-11194-0","url":null,"abstract":"<p><p>The 5-year survival rates of esophageal squamous carcinoma (ESCC) patients were pessimistic. Hsa_circ_0000419 could influence the malignant behavior of many cancers. To evaluate whether hsa_circ_0000419 can be an independent indicator for ESCC diagnosis and prognosis. Using RT-qPCR to determine hsa_circ_0000419 and miR-580-3p expression in ESCC tissues and cells. The role of hsa_circ_0000419 for ESCC patients' diagnosis and prognosis was assessed by ROC curve, Kaplan-Meier curve, and Cox regression analysis. The functions of hsa_circ_0000419 in KYSE450 and TE13 cells were tested by the CCK-8 method, transwell method, and flow cytometry. The relationship between hsa_circ_0000419 and miR-580-3p was verified by dual-luciferase reporter assay. Our study revealed that the level of hsa_circ_0000419 was elevated in ESCC tissues and cell lines. hsa_circ_0000419 ROC curves could effectively distinguish between tumor tissues and normal tissues. Kaplan-Meier curve indicated that ESCC patients had a poor prognosis with high-hsa_circ_0000419 level. The Cox regression analysis showed that hsa_circ_0000419 was an independent biomarker for ESCC. In vitro assay revealed that inhibiting hsa_circ_0000419 expression controlled the malignant behavior of ESCC, while miR-580-3p inhibitor could reverse this inhibition. hsa_circ_0000419 promoted malignant behavior in ESCC by sponging miR-580-3p. Hsa_circ_0000419 was an indicator for the diagnosis and prognosis of ESCC. Hsa_circ_0000419 promoted ESCC cell proliferation, migration, and invasion, and inhibited apoptosis by down-regulating miR-580-3p expression.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635875","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}
{"title":"Unravelling Evolutionary and Ecological Insights of Foraminifera by Using Next Generation Sequencing: A Review.","authors":"Monisha Balasubramaniyan, Yoganandan Veeran","doi":"10.1007/s10528-025-11200-5","DOIUrl":"https://doi.org/10.1007/s10528-025-11200-5","url":null,"abstract":"<p><p>Next-generation sequencing (NGS) has transformed our understanding of foraminifera biology by revealing cryptic diversity, clarifying phylogenetic relationships, and elucidating adaptive mechanisms previously inaccessible through morphological studies alone. This review delves into the potential of NGS in uncovering the secrets of foraminifera. We examine the current state of knowledge, recent breakthroughs, and future directions in applying NGS to foraminiferal research. Specifically, this study highlights how NGS enhances our understanding of foraminiferal taxonomy, adaptation to environmental changes, and functional genomics. Additionally, this review explores the potential of NGS to elucidate the genetic basis of foraminiferal shell formation, symbiotic relationships, and their responses to environmental stressors. We also address challenges and limitations associated with foraminiferal NGS, such as genome assembly complexities, intra-species heterogeneity, and sampling biases. Overall, this review aims to promote further research and collaboration in foraminiferal genomics, ultimately enhancing knowledge of these ecologically significant organisms and their contributions to marine ecosystems and paleoenvironments.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641426","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}
Ayodeji Folorunsho Ajayi, Mega Obukohwo Oyowvi, Grace Bosede Akanbi, Lydia Oluwatoyin Ajayi, Jonathan Jegede Ayomide
{"title":"Genetic Susceptibility and Pathogenesis of Hypospadias.","authors":"Ayodeji Folorunsho Ajayi, Mega Obukohwo Oyowvi, Grace Bosede Akanbi, Lydia Oluwatoyin Ajayi, Jonathan Jegede Ayomide","doi":"10.1007/s10528-025-11199-9","DOIUrl":"https://doi.org/10.1007/s10528-025-11199-9","url":null,"abstract":"<p><p>This study examines the genetic susceptibility and pathogenesis of hypospadias. Hypospadias is a birth defect of the urethra where the urinary opening is on the underside of the penis rather than at the tip. This study aims to identify the genetic basis of this defect and, by extension, improve our understanding of the biological pathways involved in its pathogenesis. Novel genetic loci and variants associated with hypospadias were identified through case-control studies in Europe and North America and, more recently, through large-scale genome-wide association studies (GWAS). The identified genetic loci may be crucial in gene regulation or expression associated with penile development, or they may increase susceptibility to environmental factors that increases the occurrence of hypospadias. Moreover, analysis of associated variants revealed that most variants have a modest effect on hypospadas risk. To better understand the underlying biological pathways, data-driven approaches such as gene expression and epigenetic analysis are being used to identify gene networks and regulatory regions relevant to hypospadias pathogenesis. In conclusion, this study provides a comprehensive overview of genetic susceptibility and pathogenesis of hypospadias and highlights the need for further research into the role of genetic and environmental factors in the onset and progression of this defect.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144635874","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}
{"title":"m<sup>6</sup>A Methylation of PODN Regulated by METTL3 Synergizes with Sorafenib to Exhibit Antitumor Function in Papillary Thyroid Cancer.","authors":"Yanlei Sun, Bolu Sun, Mei Yang, Qiangqun Deng","doi":"10.1007/s10528-025-11201-4","DOIUrl":"https://doi.org/10.1007/s10528-025-11201-4","url":null,"abstract":"<p><p>Podocan (PODN) has strong clinical diagnostic significance, and sorafenib is a versatile anti-cancer drug. Yet, neither the individual nor combined effects of PODN and sorafenib on papillary thyroid carcinoma (PTC) malignancy, nor their mechanisms, have been reported. We employed bioinformatics to pinpoint mRNAs significantly downregulated in PTC that negatively affected tumor cell migration. Using qRT-PCR, we quantified PODN and Methyltransferase-like 3 (METTL3) levels in PTC samples. MeRIP, Pearson analysis, and RIP assays validated regulatory links among PODN, METTL3, and IGF2BP1. We treated PTC cells with sorafenib or induced PODN overexpression, then assessed proliferation, migration, and invasion via CCK-8, wound healing, and Transwell assays. Both PODN and METTL3 showed low expression in PTC samples and correlated positively. Sorafenib or high PODN levels suppressed PTC cell survival, migration, and invasion. Elevated PODN also amplified sorafenib's antitumor effects in PTC cells. Moreover, METTL3 increased N6-methyladenosine (m<sup>6</sup>A) methylation of PODN, upregulating PODN mRNA and protein via an IGF2BP1-dependent mechanism. Our findings indicate that PODN inhibits PTC cell invasion, migration, and proliferation, driven by sorafenib-induced upregulation and METTL3-mediated m<sup>6</sup>A methylation. Targeting the sorafenib-METTL3-m<sup>6</sup>A-PODN synergy offers a promising new therapeutic avenue for PTC.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625111","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}
Xuebing Zhou, Liyuan Liu, Xue Wang, Dan Jiang, Xiaoliang Xie, Qi Liang, Fan Gong, Xiaoling Ding
{"title":"Study on the Effect of Antibiotics on the Efficacy of PD-1 Inhibitors and Its Regulatory Mechanism via the Intestinal Bacterial Community.","authors":"Xuebing Zhou, Liyuan Liu, Xue Wang, Dan Jiang, Xiaoliang Xie, Qi Liang, Fan Gong, Xiaoling Ding","doi":"10.1007/s10528-025-11189-x","DOIUrl":"https://doi.org/10.1007/s10528-025-11189-x","url":null,"abstract":"<p><p>This study investigated the impact of antibiotics on the therapeutic efficacy of PD-1 inhibitors and their association with the intestinal microbiota. Using a Hepa1-6 hepatocellular carcinoma mouse model, various antibiotics (vancomycin, colistin, and combination antibiotics) were administered alongside a PD-1 inhibitor. The results indicated that antibiotic treatment significantly altered the intestinal microbiota composition, with vancomycin and the combination antibiotics notably reducing PD-1 inhibitor efficacy. 16S rRNA sequencing revealed that antibiotic-induced selective pressure profoundly impacted both the diversity and abundance of the microbiota. Specifically, the relative abundance of Bacteroidetes and Firmicutes was significantly diminished following vancomycin treatment, correlating with reduced PD-1 inhibitor efficacy. Further analysis of the tumor immune microenvironment revealed no significant changes in the CD8<sup>+</sup> T cell ratio, TGF-β, IL-6, IL-17, or PD-1 levels. However, the proportion of CD4<sup>+</sup> T cells was markedly lower in the combination antibiotic group, and the expression of pro-inflammatory cytokines IFN-γ and IL-2 was substantially decreased across all antibiotic-treated groups. These findings suggest that alterations in specific intestinal bacterial populations, likely through modulation of pro-inflammatory cytokine levels in the tumor immune microenvironment, compromise immunotherapy effectiveness. This study highlights the critical role of healthy intestinal microbiota in optimizing tumor immunotherapy efficacy and emphasizes the need for careful consideration of antibiotic use in such treatments. Moreover, it provides novel insights into the mechanisms by which antibiotics may interfere with immunotherapy, laying the groundwork for optimizing anti-tumor immunotherapy strategies.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144615731","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}
Zhuanzhuan Jiang, Wanru Zhang, Ke Li, Xin Huang, Xiaojuan Li, Shao Yang
{"title":"Transcriptome Analysis Elucidates the Essential Pathways and Candidate Genes Involved in Chloroplast Development Between True Leaves and Cotyledon in Trichosanthes kirilowii Maxim.","authors":"Zhuanzhuan Jiang, Wanru Zhang, Ke Li, Xin Huang, Xiaojuan Li, Shao Yang","doi":"10.1007/s10528-025-11184-2","DOIUrl":"https://doi.org/10.1007/s10528-025-11184-2","url":null,"abstract":"<p><p>Trichosanthes kirilowii (Cucurbitaceae) is a dicotyledonous plant with morphologically and functionally distinct true leaves and cotyledons. This study integrates morphological, physiological, and transcriptomic analyses to systematically compare these two leaf types. True leaves were significantly larger, thinner, and contained higher chlorophyll a and chlorophyll b content than the smaller, thicker cotyledons. Furthermore, chloroplast thylakoid protein distribution differed between the tissues, with cotyledons enriched in low-molecular-weight chloroplast proteins. Transcriptomic profiling revealed divergent expression of genes associated with chloroplast development, including those involved in photosynthesis, pigment biosynthesis, and hormone synthesis pathways. qPCR validated key differentially expressed genes. These findings provide a comprehensive framework for understanding the molecular and functional specialization of true leaves and cotyledons in T. kirilowii, offering insights into tissue-specific chloroplast development in dicots.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144615732","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}