Aging-Us最新文献_第6页

Elucidation of the anti-colorectal cancer mechanism of Atractylodes lancea by network pharmacology and experimental verification. 通过网络药理学和实验验证阐明白术抗结直肠癌的机制

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-22 DOI: 10.18632/aging.206075

Guangliang Wang, Chuangchuang Guo, Hui Pi, Yu Wang, Shuyun Lin, Keyi Bi, Ming Zhang, Na Wang, Guojun Zhao

{"title":"Elucidation of the anti-colorectal cancer mechanism of Atractylodes lancea by network pharmacology and experimental verification.","authors":"Guangliang Wang, Chuangchuang Guo, Hui Pi, Yu Wang, Shuyun Lin, Keyi Bi, Ming Zhang, Na Wang, Guojun Zhao","doi":"10.18632/aging.206075","DOIUrl":"10.18632/aging.206075","url":null,"abstract":"Atractylodes lancea which was listed in \"Shennong's Materia Medica\" and could be used to treat gastrointestinal-associated diseases. However, its roles, core and active ingredients, and mechanisms in treatment of colorectal cancer (CRC) were still unknown. Therefore, network pharmacology and experimental validation were used to clarify the effects, core active ingredients and molecular mechanisms of Atractylodes lancea. We found that Atractylodes lancea has 28 effective active components and 213 potential targets. Seventy-three genes which demonstrate interaction between the Atractylodes lancea and CRC were confirmed. Enrichment analysis showed that 2033 GO biological process items and 144 KEGG pathways. Survival and molecular docking analysis revealed that luteolin as the core component interacted with these genes (Matrix metalloproteinase 3 (MMP3), Matrix metalloproteinase 9 (MMP9), Tissue inhibitor of metalloproteinases 1 (TIMP1), Vascular endothelial growth factor A (VEGFA)) with the lowest binding energy, and these genes were involved in building a prognostic model for CRC. Cellular phenotyping experiments showed that luteolin could inhibit the proliferation and migration of CRC cells and downregulate the expression of MMP3, MMP9, TIMP1, VEGFA probably by Phosphoinositide 3-kinase/ serine/threonine kinase Akt (PI3K/AKT) pathway. To conclude, Atractylodes lancea could inhibit proliferation and migration of CRC cells through its core active ingredient (luteolin) to suppress the expression of MMP3, MMP9, TIMP1, VEGFA probably by PI3K/AKT pathway.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142037817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Notch1 signaling pathway promotes growth and metastasis of gastric cancer via modulating CDH5. Notch1信号通路通过调节CDH5促进胃癌的生长和转移

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-21 DOI: 10.18632/aging.206061

Lingshan Zhou, Yuan Yang, Yuwei Ye, Qian Qiao, Yingying Mi, Hongfang Liu, Ya Zheng, Yuping Wang, Min Liu, Yongning Zhou

{"title":"Notch1 signaling pathway promotes growth and metastasis of gastric cancer via modulating CDH5.","authors":"Lingshan Zhou, Yuan Yang, Yuwei Ye, Qian Qiao, Yingying Mi, Hongfang Liu, Ya Zheng, Yuping Wang, Min Liu, Yongning Zhou","doi":"10.18632/aging.206061","DOIUrl":"10.18632/aging.206061","url":null,"abstract":"Objective: To explore the underlying molecular mechanism of Notch1/cadherin 5 (CDH5) pathway in modulating in cell malignant behaviors of gastric cancer (GC).Methods: We performed bioinformatic analyses to screen the potential target genes of Notch1 from cadherins in GC. Western blot and RT-PCR were conducted to detect CDH5 expression in GC tissues and cells. We utilized chromatin immunoprecipitation (CHIP) assays to assess the interaction of Notch1 with CDH5 gene. The effects of Notch1/CDH5 axis on the proliferation, invasion, migration and vasculogenic mimicry in GC cells were evaluated by EdU, wound healing, transwell, and tubule formation assays.Results: Significantly increased CDH5 expression was found in GC tissues compared with paracancerous tissues and associated to clinical stage and poor overall survival (OS) in patients with GC. Notch1 positively regulate the expression of CDH5 in GC cells. CHIP assays validated that CDH5 was a direct target of Notch1. In addition, Notch1 upregulation enhanced the proliferation, migration, invasion and vasculogenic mimicry capacity of GC cells, which could be attenuated by CDH5 silencing.Conclusions: These results indicated Notch1 upregulation enhanced GC malignant behaviors by triggering CDH5, suggesting that targeting Notch1/CDH5 axis could be a potential therapeutic strategy for GC progression.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019703","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The silent protector: Nucleoporin93's role in vascular health. 沉默的保护者核蛋白 93 在血管健康中的作用

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-21 DOI: 10.18632/aging.206097

Julia Michalkiewicz, Tung D Nguyen, Monica Y Lee

引用次数: 0

LncRNA HAGLR regulates gastric cancer progression by regulating the miR-20a-5p/E2F1 axis. LncRNA HAGLR通过调节miR-20a-5p/E2F1轴来调控胃癌的进展。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-21 DOI: 10.18632/aging.206039

Qingwei Liu, Yong Li, Bibo Tan, Qun Zhao, Liqiao Fan, Zhidong Zhang, Dong Wang, Xuefeng Zhao, Yu Liu, Wenbo Liu

{"title":"LncRNA HAGLR regulates gastric cancer progression by regulating the miR-20a-5p/E2F1 axis.","authors":"Qingwei Liu, Yong Li, Bibo Tan, Qun Zhao, Liqiao Fan, Zhidong Zhang, Dong Wang, Xuefeng Zhao, Yu Liu, Wenbo Liu","doi":"10.18632/aging.206039","DOIUrl":"10.18632/aging.206039","url":null,"abstract":"Background: Gastric cancer (GC) stands as a prevalent and challenging malignancy within the gastrointestinal tract. The potential of long non-coding RNAs (lncRNAs) as biomarkers and therapeutic targets in oncology has garnered immense research interest. This study aims to elucidate the relevance, biological roles, and mechanistic pathways of LncRNA HAGLR in the context of GC.Methods: The assessments of cell proliferation, migration, and invasion were executed using CCK-8, wound healing, and Transwell assays. The interactions between HAGLR, miR-20a-5p, and E2F1 were appraised through luciferase reporter assays, fluorescence in situ hybridization (FISH), and RNA immunoprecipitation (RIP). A tumor xenograft model provided in vivo validation for in vitro findings.Results: Elevated levels of HAGLR in GC cells and tissue specimens were linked to worse patient outcomes. The inhibition of HAGLR led to a decrease in GC cell proliferation, migration, and invasion, whereas its activation prompted contrary effects. The impact of HAGLR on cell migration and invasion was notably associated with epithelial-mesenchymal transition (EMT). Through bioinformatics, luciferase reporter assays, FISH, RIP, and Western blot analyses, it was revealed that HAGLR acts as a molecular sponge for miR-20a-5p, consequently augmenting E2F1 levels.Conclusions: The data suggest that the HAGLR/miR-20a-5p/E2F1 regulatory cascade is implicated in GC pathogenesis, offering a novel therapeutic avenue for GC management.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386921/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Acyl-CoA thioesterase 13 (ACOT13) attenuates the progression of autosomal dominant polycystic kidney disease in vitro via triggering mitochondrial-related cell apoptosis. Acyl-CoA thioesterase 13（ACOT13）通过引发线粒体相关的细胞凋亡，在体外减轻常染色体显性多囊肾病的进展。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-21 DOI: 10.18632/aging.206054

Bin Wang, Qi Yang, Lihe Che, Luyao Sun, Na Du

{"title":"Acyl-CoA thioesterase 13 (ACOT13) attenuates the progression of autosomal dominant polycystic kidney disease in vitro via triggering mitochondrial-related cell apoptosis.","authors":"Bin Wang, Qi Yang, Lihe Che, Luyao Sun, Na Du","doi":"10.18632/aging.206054","DOIUrl":"10.18632/aging.206054","url":null,"abstract":"Purpose: Autosomal dominant polycystic kidney disease (ADPKD) is the most common cause of end-stage kidney disease. It has been shown that Acyl-CoA thioesterase 13 (ACOT13) level was reduced in renal cystic tissues from ADPKD patients. However, the role of ACOT13 in ADPKD remains largely elusive.Methods: The data in the GSE7869 dataset were acquired from the GEO database to determine ACOT13 level between normal renal cortical tissues and renal cystic tissues. Next, the potential functions of ACOT13 were explored by gene set enrichment analysis (GSEA). Furthermore, ACOT13 level in ADPKD cells (WT9-12) was verified by RT-qPCR. The effects of ACOT13 on WT9-12 cell growth were evaluated using the EdU staining and flow cytometry assays.Results: Compared to normal group, ACOT13 mRNA level was obviously reduced in renal cystic tissues and WT9-12 cells. Meanwhile, GSEA results showed that compared to the low ACOT13 expression group, PI3K-Akt and MAPK signaling pathways were inactivated, and PPAR signaling pathway and fatty acid metabolism were activated in high ACOT13 expression group. Furthermore, overexpression of ACOT13 notably reduced WT9-12 cell proliferation and triggered cell cycle arrest. Moreover, ACOT13 overexpression remarkably triggered apoptosis, increased cleaved caspase 3 protein level, reduced ATP production and induced loss of mitochondrial membrane potential in WT9-12 cells, suggesting that ACOT13 overexpression could trigger mitochondrial-related apoptosis in WT9-12 cells.Conclusions: Collectively, our results showed that overexpression of ACOT13 could suppress WT9-12 cell proliferation and trigger mitochondrial-mediated cell apoptosis, suggesting that ACOT13 may exert a protective role in ADPKD.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386924/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circ_0006476 modulates macrophage apoptosis through the miR-3074-5p/DLL4 axis: implications for Notch signalling pathway regulation in cardiovascular disease. Circ_0006476通过miR-3074-5p/DLL4轴调节巨噬细胞凋亡：对心血管疾病中Notch信号通路调控的影响。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-19 DOI: 10.18632/aging.206049

Lin Cong, Lili Zhao, Ying Shi, Yunpeng Bai, Zhigang Guo

{"title":"Circ_0006476 modulates macrophage apoptosis through the miR-3074-5p/DLL4 axis: implications for Notch signalling pathway regulation in cardiovascular disease.","authors":"Lin Cong, Lili Zhao, Ying Shi, Yunpeng Bai, Zhigang Guo","doi":"10.18632/aging.206049","DOIUrl":"10.18632/aging.206049","url":null,"abstract":"As the population ages, the prevalence of atherosclerosis (AS), a significant cause of cardiovascular disease (CVD), continues to increase. Apoptosis is an independent risk factor for atherosclerosis. Macrophages are the primary immune cell group in AS lesions, and their apoptosis plays a crucial role in the occurrence and development of AS. There is a common mechanism of action for circular RNAs (circRNAs) that involves the sponging of microRNAs (miRNAs) by binding to the miRNA response element (MRE), thereby increasing the transcription of their target messenger RNAs (mRNAs). Most diseases are profoundly reliant on circRNAs. However, the underlying mechanism of circRNAs in apoptosis is yet to be elucidated. All differentially expressed genes (DEGs) and their expression levels were analysed by whole-transcriptome sequencing of samples from the control and nicotine groups of THP-1 macrophages. GO and KEGG analyses revealed that nicotine affects macrophage physiological processes and related pathways. GSEA focused on gene sets to better understand the potential pathways and biological functions of all mRNAs. A competitive endogenous RNA (ceRNA) regulatory network was constructed and validated through molecular biology experiments. The Notch signalling pathway was activated in nicotine-treated macrophages, and the expression of DLL4 in this pathway was increased. Circ_0006476 is involved in apoptosis via miR-3074-5p/DLL4, regulating pathogenic processes related to the Notch signalling pathway. The better we understand the pathways involved in macrophage apoptosis, the more likely we are to find other novel therapeutic targets that can help treat, prevent, and reduce the mortality associated with AS.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019698","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cardiac metabolism in the elderly: effects and consequences. 老年人的心脏代谢：影响和后果。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-19 DOI: 10.18632/aging.206071

Mohammad Kasim Fatmi, Nadiyeh Rouhi, Lucian Lozonschi, Ji Li

引用次数: 0

Comprehensive multi-omics analysis reveals a combination of lncRNAs that synergistically regulate glycolysis and immunotherapeutic effects in renal clear cell carcinoma. 多组学综合分析揭示了协同调控肾透明细胞癌糖酵解和免疫治疗效应的 lncRNAs 组合。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-19 DOI: 10.18632/aging.206069

Yuchen Li, Bowen Hou, Yan Xu, Hongze Li, Yuyan Zhu, Chuize Kong

{"title":"Comprehensive multi-omics analysis reveals a combination of lncRNAs that synergistically regulate glycolysis and immunotherapeutic effects in renal clear cell carcinoma.","authors":"Yuchen Li, Bowen Hou, Yan Xu, Hongze Li, Yuyan Zhu, Chuize Kong","doi":"10.18632/aging.206069","DOIUrl":"10.18632/aging.206069","url":null,"abstract":"Background: Clear cell renal carcinoma is a common urological malignancy with poor prognosis and treatment outcomes. lncRNAs are important in metabolic reprogramming and the tumor immune microenvironment, but their role in clear cell renal carcinoma is unclear.Methods: Renal clear cell carcinoma sample data from The Cancer Genome Atlas was used to establish a new risk profile by glycolysis-associated lncRNAs via machine learning. Risk profile-associated column-line plots were constructed to provide a quantitative tool for clinical practice. Patients with renal clear cell carcinoma were divided into high- and low-risk groups. Clinical features, tumor immune microenvironments, and immunotherapy responses were systematically analyzed. We experimentally confirmed the role of LINC01138 and LINC01605 in renal clear cell carcinoma.Results: The risk profile, consisting of LUCAT1, LINC01138, LINC01605, and HOTAIR, reliably predicted survival in patients with renal clear cell carcinoma and was validated in multiple external datasets. The high-risk group presented higher levels of immune cell infiltration and better immunotherapy responses than the low-risk group. LINC01138 and LINC01605 knockdown inhibited the proliferation of renal clear cell carcinoma.Conclusions: The identified risk profiles can accurately assess the prognosis of patients with clear cell renal carcinoma and identify patient populations that would benefit from immunotherapy, providing valuable insights and therapeutic targets for the clinical management of clear cell renal carcinoma.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Targeting multiple hallmarks of mammalian aging with combinations of interventions. 针对哺乳动物衰老的多种特征，采取组合干预措施。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-18 DOI: 10.18632/aging.206078

Alexander Y Panchin, Anna Ogmen, Artem S Blagodatski, Anastasia Egorova, Mikhail Batin, Timofey Glinin

{"title":"Targeting multiple hallmarks of mammalian aging with combinations of interventions.","authors":"Alexander Y Panchin, Anna Ogmen, Artem S Blagodatski, Anastasia Egorova, Mikhail Batin, Timofey Glinin","doi":"10.18632/aging.206078","DOIUrl":"10.18632/aging.206078","url":null,"abstract":"Aging is currently viewed as a result of multiple biological processes that manifest themselves independently, reinforce each other and in their totality lead to the aged phenotype. Genetic and pharmaceutical approaches targeting specific underlying causes of aging have been used to extend the lifespan and healthspan of model organisms ranging from yeast to mammals. However, most interventions display only a modest benefit. This outcome is to be expected if we consider that even if one aging process is successfully treated, other aging pathways may remain intact. Hence solving the problem of aging may require targeting not one but many of its underlying causes at once. Here we review the challenges and successes of combination therapies aimed at increasing the lifespan of mammals and propose novel directions for their development. We conclude that both additive and synergistic effects on mammalian lifespan can be achieved by combining interventions that target the same or different hallmarks of aging. However, the number of studies in which multiple hallmarks were targeted simultaneously is surprisingly limited. We argue that this approach is as promising as it is understudied.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DNA methylation-estimated phenotypes, telomere length and risk of ischemic stroke: epigenetic age acceleration of screening and a Mendelian randomization study. DNA 甲基化估计表型、端粒长度和缺血性中风风险：表观遗传学年龄加速筛查和孟德尔随机研究。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-16 DOI: 10.18632/aging.206072

Aierpati Maimaiti, Jianhua Ma, Chenguang Hao, Dengfeng Han, Yongxin Wang, Zengliang Wang, Rena Abudusalamu

{"title":"DNA methylation-estimated phenotypes, telomere length and risk of ischemic stroke: epigenetic age acceleration of screening and a Mendelian randomization study.","authors":"Aierpati Maimaiti, Jianhua Ma, Chenguang Hao, Dengfeng Han, Yongxin Wang, Zengliang Wang, Rena Abudusalamu","doi":"10.18632/aging.206072","DOIUrl":"10.18632/aging.206072","url":null,"abstract":"Background: Aging is a complex biological process that may be accelerated in certain pathological conditions. DNA methylation age (DNAmAge) has emerged as a biomarker for biological age, which can differ from chronological age. This research peels back the layers of the relationship between fast-forward aging and ischemic stroke, poking and prodding the potential two-way causal influences between stroke and biological aging indicators.Methods: We analyzed a cohort of ischemic stroke patients, comparing DNAmAge with chronological age to measure age acceleration. We assessed variations in age acceleration among stroke subtypes and between sexes. Using Mendelian randomization, we examined the causal links between stroke, aging biomarkers like telomere length, and age acceleration's effect on stroke risk.Results: Our investigation reveals a pronounced association between ischemic stroke and age acceleration, most notably in patients with cardioembolic strokes, who exhibited a striking median difference of 9 years between DNAmAge and chronological age. Furthermore, age acceleration differed significantly across stroke subtypes and was higher in women than in men. In terms of causality, MR analysis indicated a modest negative effect of stroke on telomere length, but no causal effect of age phenotypes on stroke or its subtypes. However, some indication of a potential causal effect of ischemic stroke on PhenoAge acceleration was observed.Conclusion: The study provides insight into the relationship between DNAmAge and ischemic stroke, particularly cardioembolic stroke, and suggests possible gender differences. These insights carry profound clinical significance and set stage for future investigations into the entwined pathways of stroke and accelerated aging.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11386914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0