Biochemistry and Cell Biology最新文献_第4页

CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway. CD38 缺乏症可通过激活 SIRT3 途径抑制脂质积累和氧化应激，从而预防糖尿病肾病。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-08-08 DOI: 10.1139/bcb-2024-0058

Ling-Fang Wang, Qian Li, Jia Le Zhao, Ke Wen, Ya-Ting Zhang, Qi-Hang Zhao, Qi Ding, Jia-Hui Li, Xiao-Hui Guan, Yun-Fei Xiao, Ke-Yu Deng, Hong-Bo Xin

{"title":"CD38 deficiency prevents diabetic nephropathy by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.","authors":"Ling-Fang Wang, Qian Li, Jia Le Zhao, Ke Wen, Ya-Ting Zhang, Qi-Hang Zhao, Qi Ding, Jia-Hui Li, Xiao-Hui Guan, Yun-Fei Xiao, Ke-Yu Deng, Hong-Bo Xin","doi":"10.1139/bcb-2024-0058","DOIUrl":"10.1139/bcb-2024-0058","url":null,"abstract":"Diabetic nephropathy (DN) is one of the most common complications of diabetes. Our previous study showed that CD38 knockout (CD38KO) mice had protective effects on many diseases. However, the roles and mechanisms of CD38 in DN remain unknown. Here, DN mice were generated by high-fat diet (HFD) feeding plus streptozotocin (STZ) injection in male CD38KO and CD38flox mice. Mesangial cells (SV40 MES 13 cells) were used to mimic the injury of DN with palPagination Donemitic acid (PA) treatment in vitro. Our results showed that CD38 expression was significantly increased in kidney of diabetic CD38flox mice and SV40 MES 13 cells treated with PA. CD38KO mice were significantly resistant to diabetes-induced renal injury. Moreover, CD38 deficiency markedly decreased HFD/STZ-induced lipid accumulation, fibrosis, and oxidative stress in kidney tissue. In contrast, overexpression of CD38 aggravated PA-induced lipid accumulation and oxidative stress. CD38 deficiency increased expression of SIRT3, while overexpression of CD38 decreased its expression. More importantly, 3-TYP, an inhibitor of SIRT3, significantly enhanced PA-induced lipid accumulation and oxidative stress in CD38 overexpressing cell lines. In conclusion, our results demonstrated that CD38 deficiency prevented DN by inhibiting lipid accumulation and oxidative stress through activation of the SIRT3 pathway.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141905787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells. NFIB在乳腺癌上皮细胞长期雌激素治疗导致的SOX2下调和表观基因组可及性改变中的作用

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0287

Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell

{"title":"A role for NFIB in SOX2 downregulation and epigenome accessibility changes due to long-term estrogen treatment of breast cancer epithelial cells.","authors":"Luis E Abatti, Zoe E Gillespie, Patricia Lado-Fernández, Manuel Collado, Jennifer A Mitchell","doi":"10.1139/bcb-2024-0287","DOIUrl":"10.1139/bcb-2024-0287","url":null,"abstract":"Estrogen (E2) regulates the differentiation and proliferation of mammary progenitor cells by modulating the transcription of multiple genes. One of the genes that is downregulated by E2 is SOX2, a transcription factor associated with stem and progenitor cells that is overexpressed during breast tumourigenesis. To elucidate the mechanisms underlying E2-mediated SOX2 repression, we investigated epigenome and transcriptome changes following short- and long-term E2 exposure in breast cancer cells. We found that short-term E2 exposure reduces chromatin accessibility at the downstream SOX2 SRR134 enhancer, decreasing SOX2 expression. In contrast, long-term E2 exposure completely represses SOX2 transcription while maintaining accessibility at the SRR124-134 enhancer cluster, keeping it poised for reactivation. This repression was accompanied by widespread epigenome and transcriptome changes associated with commitment towards a more differentiated and less invasive luminal phenotype. Finally, we identified a role for the transcription factor NFIB in this process, suggesting it collaborates with the estrogen receptor to mediate SOX2 repression and genome-wide epigenome accessibility changes.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-14"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Perturbation of calcium homeostasis invokes eryptosis-like cell death in enucleated bone marrow stem cells. 扰乱钙稳态会导致无核骨髓干细胞发生红细胞增多症样细胞死亡。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-18 DOI: 10.1139/bcb-2024-0106

Wei Yan, Ruolan Wu, Yingying Lee, Liqun Xu, Xiao Li, Junwei Li, Ronghao Deng, Xing Fan, Yilang Wu, Haibao Zhu, Aihua Mao, Jianxin Shen, Chi-Ju Wei

{"title":"Perturbation of calcium homeostasis invokes eryptosis-like cell death in enucleated bone marrow stem cells.","authors":"Wei Yan, Ruolan Wu, Yingying Lee, Liqun Xu, Xiao Li, Junwei Li, Ronghao Deng, Xing Fan, Yilang Wu, Haibao Zhu, Aihua Mao, Jianxin Shen, Chi-Ju Wei","doi":"10.1139/bcb-2024-0106","DOIUrl":"10.1139/bcb-2024-0106","url":null,"abstract":"Enucleated cells, also known as cytoplasts, are valuable tools with a wide range of applications. However, their potential for bio-engineering is greatly restricted by the short lifespan. We postulated that the enucleation process damages the integrity of the plasma membrane and thus activates a cell death program(s). The results showed that a tiny hole was generated transiently on the plasma membrane when the nucleus was spun off, while force-gated ion channels were activated in response to the pulling by the nucleus. Influx of extracellular calcium stimulated the opening of calcium channels and the release of calcium from endoplasmic reticulum and mitochondria. Long lasting calcium transient increased protein phosphorylation and activated caspase 9 and calpain proteinase activities. Subsequently, mitochondria membrane permeability and Reactive Oxygen Species (ROS) levels were significantly elevated, which eventually led to eryptosis-like cell death. When extracellular calcium was maintained at optimal concentration, the lifespan of enucleated cells was extended; however, huge amounts of vacuoles appeared in the cytoplasm, possibly derived from enlarged autophagosomes. Inhibition of vacuolation by inhibitors of autophagy or in co-culture with primary muscle cells did not rescue cells dying from the paraptosis-like pathway. These results offer valuable insights for further investigation into the intricate mechanisms underlying enucleated cell death.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway. WDR4通过激活GSK3β/β-catenin通路促进结直肠癌的进展。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0168

Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu

{"title":"WDR4 promotes colorectal cancer progression by activating the GSK3β/β-catenin pathway.","authors":"Hongyu Wang, Liyang Liang, Yanfei Wang, Xuan Zhong, Chao Zhang, Zhipeng Liu, Jinzhong Liu, Wanning Hu","doi":"10.1139/bcb-2024-0168","DOIUrl":"10.1139/bcb-2024-0168","url":null,"abstract":"WD repeat domain 4 (WDR4) has been reported to promote tumor metastasis in various cancers. However, its precise function in colorectal cancer (CRC) has not been reported yet. Herein, the expression pattern of WDR4 in CRC was determined by analyzing Gene Expression Omnibus datasets (GSE110225, GSE127069, GSE156355, and GSE184093) and GEPIA online dataset. In vitro and in vivo experiments, including CCK-8, colony formation, flow cytometry, wound healing, transwell assays, and xenograft mouse models, were used to investigate the role of WDR4 in CRC. Firstly, data from Kaplan-Meier database showed that high expression of WDR4 was associated with the poor prognosis of CRC patients. Then, upregulation of WDR4 was confirmed in clinical CRC tissues. In vitro functional experiments suggested that overexpression of WDR4 promoted cell proliferation, migration, and invasion, while knockdown of WDR4 has the opposite effects. Also, the oncogenic role of WDR4 was also verified in in vivo experiments. CO-IP-LC/MS analysis uncovered that glycogen synthase kinase 3β (GSK3β) is the central protein that binds to WDR4. Mechanistically, WDR4 activated the β-catenin pathway by promoting GSK3β phosphorylation. This study demonstrates that WDR4 promotes CRC progression through activating GSK3β/β-catenin pathway, indicating that WDR4 might be a potential therapeutic target for CRC treatment.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Retraction: Long noncoding RNA HIF1A-AS2 facilitates cell survival and migration by sponging miR-33b-5p to modulate SIRT6 expression in osteosarcoma. 缩稿：长链非编码RNA HIF1A-AS2通过海绵miR-33b-5p调节SIRT6在骨肉瘤中的表达，促进细胞存活和迁移。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2025-0019

引用次数: 0

Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes. Omega-3多不饱和脂肪酸改变THP-1单核细胞的葡萄糖代谢。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0202

Michael J Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha D Pauls

{"title":"Omega-3 polyunsaturated fatty acids modify glucose metabolism in THP-1 monocytes.","authors":"Michael J Byun, Roni Armon, Tamiris F G Souza, Hope D Anderson, Ayesha Saleem, Samantha D Pauls","doi":"10.1139/bcb-2024-0202","DOIUrl":"10.1139/bcb-2024-0202","url":null,"abstract":"Chronic inflammation is a driving factor in diseases like obesity and type 2 diabetes. Enhanced cellular glucose metabolism may contribute to heightened immune activation. A human supplementation trial showed that the n-3 PUFA α-linolenic acid (ALA) reduced oxidative phosphorylation in monocytes. Our objective here is to assess the direct effects of ALA and docosahexaenoic acid (DHA) on glucose metabolism in a cell culture model and to explore possible molecular mechanisms. THP-1 monocytes were treated with 10-40 µmol/L of ALA or DHA and compared with vehicle and oleic acid controls. The Seahorse XFe24 and Oroboros O2k Oxygraph systems were used to approximate catabolic rates in the presence of glucose. Both ALA and DHA reduced oxidative phosphorylation. We identified pyruvate dehydrogenase kinase 4 (PDK4) as a possible mechanistic candidate explaining the effect of DHA. Additionally, both n-3 PUFAs reduced lipopolysaccharides-induced IL-1β production, while only DHA increased reactive oxygen species to a small but significant extent. Our data suggest that ALA and DHA trigger a re-wiring of bioenergetic pathways in monocytes, possibly via the upregulation of PDK4. Given the close relationship between cell metabolism and immune cell activation, this may represent a novel mechanism by which n-3 fatty acids modulate immune function and inflammation.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-10"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143121857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Note of appreciation. 表示感谢。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0284

引用次数: 0

Hydrocortisone improves post-resuscitation myocardial dysfunction by inhibiting the NF-κB pathway. 氢化可的松通过抑制 NF-κB 通路改善复苏后心肌功能障碍。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-11-13 DOI: 10.1139/bcb-2024-0162

Yaqin Fang, Fenglin Song, Chunyan Gao, Zhiming Wang

{"title":"Hydrocortisone improves post-resuscitation myocardial dysfunction by inhibiting the NF-κB pathway.","authors":"Yaqin Fang, Fenglin Song, Chunyan Gao, Zhiming Wang","doi":"10.1139/bcb-2024-0162","DOIUrl":"10.1139/bcb-2024-0162","url":null,"abstract":"Myocardial dysfunction is a major cause of early mortality after successful cardiopulmonary resuscitation (CPR) following cardiac arrest (CA). Following the return of spontaneous circulation, myocardial ischemia-reperfusion injury can activate the NF-κB pathway, leading to the transcription of inflammatory genes that impair myocardial function. While clinical studies show hydrocortisone (HC) improves outcomes in CA patients during CPR, its specific role in modulating the NF-κB pathway is unclear. In this study, we established an in vitro model by inducing hypoxia/reoxygenation (H/R) injury in H9C2 cardiomyocytes using Na2S2O4, followed by HC treatment. The results showed that HC treatment of H/R-injured cardiomyocytes promoted proliferation, inhibited apoptosis, and suppressed the NF-κB pathway, thereby reducing interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) levels. Moreover, inhibition of the NF-κB pathway enhanced the proliferative capacity of H/R cardiomyocytes, decreased apoptosis rates, and reduced IL-6, IL-8, and TNF-α expression levels, with these effects being further amplified by HC treatment. These findings were further supported by in vivo experiments. In conclusion, our study suggests that HC may promote H/R cardiomyocyte proliferation, inhibit apoptosis, and alleviate inflammatory responses by suppressing the NF-κB pathway, providing new evidence to support its potential clinical application in CA management.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-11"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Treatment of lactoferrin and antimicrobial peptide N6 on bacterial enteritis caused by Escherichia coli in mice. 乳铁蛋白和抗菌肽 N6 对大肠杆菌引起的小鼠细菌性肠炎的治疗作用。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 Epub Date: 2024-10-11 DOI: 10.1139/bcb-2024-0103

Xuanxuan Ma, Kun Zhang, Na Yang, Ya Hao, Ruoyu Mao, Da Teng, Jianhua Wang

{"title":"Treatment of lactoferrin and antimicrobial peptide N6 on bacterial enteritis caused by Escherichia coli in mice.","authors":"Xuanxuan Ma, Kun Zhang, Na Yang, Ya Hao, Ruoyu Mao, Da Teng, Jianhua Wang","doi":"10.1139/bcb-2024-0103","DOIUrl":"10.1139/bcb-2024-0103","url":null,"abstract":"Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhea in humans and animals. The study aimed to evaluate the efficacy of bovine lactoferrin (bLf) as an adjuvant combined with AMP (N6) in the treatment of E. coli-induced bacterial enteritis. Firstly, 40 female ICR mice were randomly divided into four groups. The ETEC-A, ETEC-B, and ETEC-C groups were gavaged with 0.2 mL of ETEC K88 at 5 × 109, 5 × 108, and 5 × 107 CFU/mL for three consecutive days, respectively, the CK control group was given PBS. Based on the clinical symptoms and intestinal changes, the optimal model dose of ETEC K88 was determined to be 5 × 108 CFU/mL. Sixty female ICR mice were randomly divided into six groups: CK group (uninfected), NC group (infected and untreated), N6 treatment group (20 mg/kg), bLf treatment group (100 mg/kg), bLf + N6-A treatment group (10 mg/kg N6+100 mg/kg bLf), and bLf + N6-B group (20 mg/kg N6+100 mg/kg bLf). The clinical symptoms, intestinal morphology, inflammatory response and serum metabolites were monitored. The results showed that compared with the NC group, the bLf-N6-A and bLf-N6-B treatment groups had significant reductions in TNF-α and IL-6, significant increases in IL-10, and significant reductions in endotoxin and DAO in plasma (p < 0.05). Meanwhile, the bLf-N6-A and bLf-N6-B treatment groups significantly increased the expression of ZO-1, claudin-1 and occludin, increased the height of small intestinal mucosal villi and VH/CD after ETEC K88-induced intestinal injury (p < 0.05). The combination of bLf and N6 relieved enteritis by balancing intestinal mucosal immunity, improving intestinal morphology and barrier function. BLf combined with N6 can be used as an effective therapeutic strategy for the treatment of bacterial enteritis.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142405978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Effects of different sources of lactoferrin on cytokine response to SARS-COV-2, respiratory syncytial virus, and rotavirus infection in vitro. 不同来源的乳铁蛋白对体外 SARS-COV-2、呼吸道合胞病毒和轮状病毒感染的细胞因子反应的影响。

IF 2.4 3区生物学

Biochemistry and Cell Biology Pub Date : 2025-01-01 DOI: 10.1139/bcb-2024-0146

Rulan Jiang, Xiaogu Du, Bo Lönnerdal

{"title":"Effects of different sources of lactoferrin on cytokine response to SARS-COV-2, respiratory syncytial virus, and rotavirus infection in vitro.","authors":"Rulan Jiang, Xiaogu Du, Bo Lönnerdal","doi":"10.1139/bcb-2024-0146","DOIUrl":"10.1139/bcb-2024-0146","url":null,"abstract":"Lactoferrin (Lf) is a multifunctional iron-binding glycoprotein, involved in a wide range of bioactivities, including immunomodulatory and antiviral activities. Lf in human milk and bovine Lf added to infant formula may provide some protection against viral infections. However, functions of Lfs from different sources may differ due to varying manufacturing processes and posttranslational modifications. Here, effects of Lfs (11 commercial bovine milk Lfs, 2 recombinant Lfs, and native human/bovine milk Lf) on cytokine responses to virus infection were examined by infecting human intestinal epithelial cells (Caco-2 cells) with rotavirus (naked) or normal human bronchial epithelial cells (BEAS-2B cells) with respiratory syncytial virus (RSV, enveloped) or severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike protein 1. Effects of Lf on viral infection were evaluated by quantitative real-time polymerase chain reaction analysis of transcripts of cytokines/chemokines (TNF-α, IL-1β, IL-6, IL-8, IL-10, IFN-β, and CXCL10). Our results show that viral infection changes transcription of these cytokines and that Lfs significantly and variously influence immune responses to rotavirus, RSV, and SARS-CoV-2 in vitro. Thus, Lf may provide protection against virus infection by down-regulating pro-inflammatory cytokine/chemokine responses. Recombinant bovine and human Lf show similar effects as bovine milk Lfs suggesting that different posttranslational modifications do not affect the antiviral activity on cytokine response.","PeriodicalId":8775,"journal":{"name":"Biochemistry and Cell Biology","volume":" ","pages":"1-12"},"PeriodicalIF":2.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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