Epigenomics最新文献

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Epigenetic age acceleration and psychosocial stressors in early childhood. 儿童早期的表观遗传年龄加速和社会心理压力。
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 Epub Date: 2025-06-02 DOI: 10.1080/17501911.2025.2508684
Connie J Mulligan
{"title":"Epigenetic age acceleration and psychosocial stressors in early childhood.","authors":"Connie J Mulligan","doi":"10.1080/17501911.2025.2508684","DOIUrl":"10.1080/17501911.2025.2508684","url":null,"abstract":"<p><p>The impact of psychosocial stress on mental and physical health is well-documented. Adverse experiences that occur early in life are particularly impactful on later life health. Epigenetic modifications, such as DNA methylation, have been proposed as a possible mechanism to mediate the impact of childhood events on adult health outcomes. The development of epigenetic clocks to estimate epigenetic age has revealed many examples of epigenetic age acceleration (and deceleration) in association with exposure to psychosocial stressors. Furthermore, altered epigenetic aging has been associated with downstream health outcomes. Here studies are discussed that have reported associations of epigenetic aging with early-life exposure to psychosocial stressors, such as childhood abuse and neglect, and with later-life health outcomes, including increased mortality, morbidity, and disease risk. Protective factors that may mitigate the effect of psychosocial stress on epigenetic aging, and possibly enable reversal of epigenetic aging, are also discussed.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"701-710"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144198608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Correction. 修正。
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 Epub Date: 2025-06-26 DOI: 10.1080/17501911.2025.2523710
{"title":"Correction.","authors":"","doi":"10.1080/17501911.2025.2523710","DOIUrl":"10.1080/17501911.2025.2523710","url":null,"abstract":"","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"I"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495335","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Personalized medicine for cardiovascular diseases: how next generation epigenetic technologies can contribute? 心血管疾病的个体化治疗:下一代表观遗传技术如何发挥作用?
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 Epub Date: 2025-06-14 DOI: 10.1080/17501911.2025.2518917
Meeshanthini Dogan, Robert Philibert
{"title":"Personalized medicine for cardiovascular diseases: how next generation epigenetic technologies can contribute?","authors":"Meeshanthini Dogan, Robert Philibert","doi":"10.1080/17501911.2025.2518917","DOIUrl":"10.1080/17501911.2025.2518917","url":null,"abstract":"<p><p>Advances in DNA methylation and artificial intelligence have led to new methods for assessing risk and diagnosing coronary heart disease (CHD), the leading cause of death. However, whether these technologies can also be harnessed to generate new pharmacotherapeutic agents or monitor the effectiveness of new or existing CHD therapies is unknown. In this perspective, we review the development of cardiac assessment technologies and the challenges that these older approaches attempted to address. We next describe Precision Epigenetic methods and describe their strengths and limitations, as well as the conceptual framework through which these tools operate. Finally, we discuss their potential application to the development and evaluation of new therapies for CHD and how Precision Epigenetic tools compare to existing testing modalities for CHD. We conclude that the future is bright for the use of Precision Epigenetic methods in cardiovascular medicine and suggest that their routine use could lead to faster, less expensive and more effective healthcare.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"675-680"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Microglial immune memory in Parkinson's and Huntington's diseases: epigenetics, triggers, and therapies. 帕金森病和亨廷顿病的小神经胶质免疫记忆:表观遗传学、触发因素和治疗方法。
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 DOI: 10.1080/17501911.2025.2518909
Reema Chowdhury, Anna Hendlinger, Olaf Riess, Julia Schulze-Hentrich
{"title":"Microglial immune memory in Parkinson's and Huntington's diseases: epigenetics, triggers, and therapies.","authors":"Reema Chowdhury, Anna Hendlinger, Olaf Riess, Julia Schulze-Hentrich","doi":"10.1080/17501911.2025.2518909","DOIUrl":"https://doi.org/10.1080/17501911.2025.2518909","url":null,"abstract":"<p><p>Neurodegenerative disorders, like Parkinson's and Huntington's disease, have a profound global impact but currently lack effective treatments. Accumulations of misfolded proteins of <i>α</i>-synuclein and huntingtin are a common pathological hallmark in these diseases, respectiveley. Recently, the role of microglia and innate immune memory in modulating neurodegenerative diseases has been studied in more detail. This review explores the mechanisms of microglial activation in Parkinson's and Huntington's, emphasizing innate immune memory, epigenetic reprogramming, and the influence of external triggers such as lipopolysaccharides (LPS) and high-fat diets (HFD). The review also examines therapeutic strategies targeting microglia to mitigate neurodegeneration, including shifting microglial phenotypes from pro-inflammatory to anti-inflammatory states using epigenetic interventions. To support this review, a structured literature search was conducted using PubMed, Scopus, and Web of Science. Keywords included microglia, innate immune memory, epigenetics, neuroinflammation, and disease-specific terms. Future research should focus on improving animal models, investigating environmental stressors, and developing reliable biomarkers to strengthen translational approaches for neuroinflammatory-driven neurodegenerative diseases.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-14"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144539640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
DNMT1/MTTP axis promotes gastritis progression during Helicobacter pylori infection by regulating GPX4 and ferroptosis. DNMT1/MTTP轴通过调节GPX4和铁下垂促进幽门螺杆菌感染期间胃炎的进展。
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 Epub Date: 2025-06-09 DOI: 10.1080/17501911.2025.2510187
Chunli Tang, Fanlai Meng, Renjie Li, Meimei Ma, Meiling Zhu, Chunfang Xu
{"title":"DNMT1/MTTP axis promotes gastritis progression during <i>Helicobacter pylori</i> infection by regulating GPX4 and ferroptosis.","authors":"Chunli Tang, Fanlai Meng, Renjie Li, Meimei Ma, Meiling Zhu, Chunfang Xu","doi":"10.1080/17501911.2025.2510187","DOIUrl":"10.1080/17501911.2025.2510187","url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori (H. pylori)</i>-induced chronic atrophic gastritis (CAG) is a significant health concern. The role of microsomal triglyceride transfer protein (MTTP) in CAG progression has not been explored, presenting a critical knowledge gap in understanding <i>H. pylori</i>-induced CAG pathogenesis.</p><p><strong>Methods: </strong>Sprague-Dawley rats and gastric epithelial cell line were infected with H. pylori to build CAG model. The mRNA and protein levels of DNA methyltransferase 1 (DNMT1), MTTP, and glutathione peroxidase 4 (GPX4) were measured by quantitative real-time PCR (RT-qPCR) and western blotting, respectively. Moreover, the localization of DNMT1 and MTTP was detected via immunohistochemistry. Furthermore, the pathological changes of gastric tissue were analyzed by HE staining.</p><p><strong>Results: </strong>The MTTP expression was downregulated in CAG. Moreover, overexpression of MTTP in gastric epithelial cells could suppress the inflammatory response induced by <i>H. pylori</i> infection and ferroptosis by upregulating GPX4 expression. In addition, DNMT1 expression was upregulated in CAG and was negatively correlated with MTTP expression. Furthermore, DNMT1 could target MTTP promoter to activate methylation and downregulate MTTP expression.</p><p><strong>Conclusion: </strong>DNMT1 downregulated the MTTP expression through methylation, and thus mediate inflammasome-ferroptosis processes via GPX4 in the <i>H. pylori</i>-induced CAG.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"647-659"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144247087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Regulatory roles of transposable elements on autism molecular neuropathology. 转座因子在自闭症分子神经病理学中的调控作用。
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 Epub Date: 2025-05-06 DOI: 10.1080/17501911.2025.2501520
Peerapa Techaniyom, Chawin Korsirikoon, Pitaksin Chitta, Chanachai Sae-Lee
{"title":"Regulatory roles of transposable elements on autism molecular neuropathology.","authors":"Peerapa Techaniyom, Chawin Korsirikoon, Pitaksin Chitta, Chanachai Sae-Lee","doi":"10.1080/17501911.2025.2501520","DOIUrl":"10.1080/17501911.2025.2501520","url":null,"abstract":"<p><p>Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by challenges in social communication and the presence of repetitive behaviors, typically diagnosed in early childhood. In this review, we searched PubMed and Google Scholar databases for relevant articles. ASD displays considerable heterogeneity in symptomatology and is more common in males, though shifting demographics indicate rising rates among minority populations. Transposable elements (TEs), which constitute approximately 50% of the mammalian genome, are increasingly recognized for their contribution to neurodevelopmental disorders, including ASD. These mobile genetic elements can induce genomic instability and modulate gene expression, thereby influencing ASD pathology. Evidence suggests that specific TEs, such as L1 and <i>Alu</i> elements, can disrupt genes critical for neurodevelopment and contribute to the disorder's genetic complexity. Furthermore, prenatal environmental exposures may activate TEs, potentially contributing to neuroinflammation observed in ASD. While the precise regulatory roles of non-coding TEs in ASD are still under investigation and require careful interpretation, integrating epigenetic aging markers like epigenetic clocks holds promise for advancing the field. Future research focused on the intricate relationship between TEs, environmental factors, epigenetic mechanisms, and neurodevelopmental processes is essential for identifying novel biomarkers and therapeutic targets, ultimately improving early diagnosis and interventions for ASD.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"691-699"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980468","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 epigenetic potential of vitamin K2 in brain health. 维生素K2对大脑健康的表观遗传潜力。
IF 3 4区 医学
Epigenomics Pub Date : 2025-07-01 Epub Date: 2025-06-12 DOI: 10.1080/17501911.2025.2518916
Stefanos Roumeliotis, Rosaria A Cavallaro, Ioannis Kontogiorgos, Ioannis E Neofytou, Katarzyna Maresz, Jean-Francois Jeanne, Niccolò Miraglia, Andrea Fuso
{"title":"The epigenetic potential of vitamin K2 in brain health.","authors":"Stefanos Roumeliotis, Rosaria A Cavallaro, Ioannis Kontogiorgos, Ioannis E Neofytou, Katarzyna Maresz, Jean-Francois Jeanne, Niccolò Miraglia, Andrea Fuso","doi":"10.1080/17501911.2025.2518916","DOIUrl":"10.1080/17501911.2025.2518916","url":null,"abstract":"<p><p>Vitamin K2 refers to a subfamily of vitamin K isoforms known as Menaquinones and, therefore, indicated as MK-n, the \"n\" indicating the number of isoprene units present in the side chain. Like the other members of the Vitamin K family, K2 is an enzymatic cofactor for the γ-glutamyl carboxylase (GGCX). This enzyme's substrates, which carboxylate glutamic acid residues, are known as Vitamin K-dependent proteins (VKDPs). Besides being involved in bone homeostasis, vitamin K exerts its primary function in the coagulation process. More recently, a function of Vitamin K also in brain homeostasis has been claimed. In addition to these so-called \"canonical\" effects, recent research highlights the possibility that Vitamin K, particularly Vitamin K2 May 2001have or induce epigenetic effects through the modulation of DNA methylation, histone modifications, and microRNAs expression. This evidence seems particularly relevant in brain diseases, where epigenetics is gaining a central role as a modulator of multiple diseases-associated molecular metabolisms. The present review examines the recent literature (PubMed) to collect evidence for the role of Vitamin K2 in neurodegenerative diseases with the goal of fostering interest in its epigenetic potential.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"681-690"},"PeriodicalIF":3.0,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12233872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
HTR2A DNA methylation as a diagnostic biomarker for rheumatoid arthritis: a validation study using targeted sequencing. HTR2A DNA甲基化作为类风湿关节炎的诊断生物标志物:一项使用靶向测序的验证研究
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-27 DOI: 10.1080/17501911.2025.2523231
Jianan Zhao, Binghen He, Yunshen Li, Yu Shan, Kai Wei, Ping Jiang, Yiming Shi, Yixin Zheng, Fuyu Zhao, Guizhen Yang, Qianqian Li, Mi Zhou, Shicheng Guo, Yuejuan Zheng, Juan Jiao, Rongsheng Wang, Cen Chang, Liangjing Lv
{"title":"<i>HTR2A</i> DNA methylation as a diagnostic biomarker for rheumatoid arthritis: a validation study using targeted sequencing.","authors":"Jianan Zhao, Binghen He, Yunshen Li, Yu Shan, Kai Wei, Ping Jiang, Yiming Shi, Yixin Zheng, Fuyu Zhao, Guizhen Yang, Qianqian Li, Mi Zhou, Shicheng Guo, Yuejuan Zheng, Juan Jiao, Rongsheng Wang, Cen Chang, Liangjing Lv","doi":"10.1080/17501911.2025.2523231","DOIUrl":"https://doi.org/10.1080/17501911.2025.2523231","url":null,"abstract":"<p><strong>Objectives: </strong>To validate the potential of the serotonin receptor encoded by 5-hydroxytryptamine receptor 2A (HTR2A) cg15692052 DNA methylation as a diagnostic biomarker for rheumatoid arthritis (RA) and its subtypes.</p><p><strong>Methods: </strong>MethylTarget<sup>TM</sup> targeted region methylation sequencing technology was employed to analyze the DNA methylation levels of HTR2A cg15692052 in RA, health control, ankylosing spondylitis, psoriatic arthritis, gout, systemic lupus erythematosus, dermatomyositis, and primary Sjögren's syndrome patients within the region of chr13:46898190~chr13:46897976. Machine learning algorithms were used to analyze data.</p><p><strong>Results: </strong>Compared to the HC group, RA patients and four serological subtypes of RA (RF-negative RA, RF/CCP double-positive, RF/CCP double-negative, and CCP-negative RA) exhibited significantly higher levels of <i>HTR2A</i> cg15692052 methylation (<i>p</i> < 0.05). Methylation levels in RA patients and its four serological subtypes were significantly positively correlated with erythrocyte sedimentation rate or C-reactive protein (<i>p</i> < 0.05). <i>HTR2A</i> cg15692052 methylation levels combined with different clinical features can significantly distinguish RA patients with AUCs ranging from 0.672 to 0.757, RF/CCP double-negative patients with AUCs from 0.825 to 0.966, RF/CCP double-positive RA patients with AUCs from 0.714 to 0.846, and RF-negative RA patients with AUCs from 0.928 to 0.932.</p><p><strong>Conclusions: </strong>The <i>HTR2A</i> cg15692052 DNA methylation level can serve as a diagnostic biomarker for RA and its subtypes.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-11"},"PeriodicalIF":3.0,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144505237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Techniques to detect physical interactions between genomic regions. 检测基因组区域间物理相互作用的技术。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-26 DOI: 10.1080/17501911.2025.2523232
Takayuki Hata, Hodaka Fujii
{"title":"Techniques to detect physical interactions between genomic regions.","authors":"Takayuki Hata, Hodaka Fujii","doi":"10.1080/17501911.2025.2523232","DOIUrl":"https://doi.org/10.1080/17501911.2025.2523232","url":null,"abstract":"<p><p>Chromatin forms specific intranuclear structures through physical interactions between specific genomic regions mediated by DNA-binding proteins and/or RNAs. Recent efforts have revealed that these genome organizations and dynamics are involved in various functions of genomic DNA, such as regulation of gene expression, DNA replication, cell division, and epigenetic memory, which are mechanisms underlying cell differentiation and disease development. The methods to detect physically interacting chromatin regions and reconstruct 3D genomic organization can be roughly categorized into four types: (i) microscopic observation of visualized intranuclear structures, (ii and iii) sequencing-based methods including proximity ligation-dependent/independent methods, and (iv) <i>de novo</i> prediction from genomic sequences and other omics data. Here, we review these techniques to detect physical interactions between genomic regions, highlighting their unique advantages and limitations.</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-13"},"PeriodicalIF":3.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144495336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Accurate interpretation of inosines in RNAs: recognized as G is more than basepairing with C. 准确解释rna中的肌苷:识别为G的不仅仅是与C进行碱基修复。
IF 3 4区 医学
Epigenomics Pub Date : 2025-06-21 DOI: 10.1080/17501911.2025.2523237
Yuange Duan
{"title":"Accurate interpretation of inosines in RNAs: recognized as G is more than basepairing with C.","authors":"Yuange Duan","doi":"10.1080/17501911.2025.2523237","DOIUrl":"10.1080/17501911.2025.2523237","url":null,"abstract":"<p><p>Adenosine-to-inosine (A-to-I) mRNA editing epigenetically mimics A-to-G mutations. While literatures usually state \"inosines are recognized as guanosines,\" sometimes we also see expressions like \"inosines basepair with cytosines.\" In this article, I stress that the two expressions are not equivalent at all for the following reasons. (1) inosines are recognized as guanosines only when located in mRNAs, not tRNAs; (2) even when being recognized as guanosines, inosines can basepair with cytosine and uracil; (3) when inosine pairs with cytosine, the basepairing efficiency differs from G:C pairing. Therefore, we should be cautious when introducing A-to-I RNA editing. \"inosines basepair with cytosines\" is an inaccurate or incomplete interpretation and should be corrected as \"inosines in mRNAs are recognized as guanosines.\"</p>","PeriodicalId":11959,"journal":{"name":"Epigenomics","volume":" ","pages":"1-6"},"PeriodicalIF":3.0,"publicationDate":"2025-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144339991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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