Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis最新文献

{"title":"The mechanism underlying the oncogenic potential of AAA+ ATPase PSMC4 in cancer is revealed by mutations and copy number amplifications","authors":"Sanjida Mallick ,&nbsp;Qurratulain Qamar ,&nbsp;Bibhudutta Mishra ,&nbsp;Aditi Nayak","doi":"10.1016/j.mrfmmm.2025.111901","DOIUrl":"10.1016/j.mrfmmm.2025.111901","url":null,"abstract":"<div><div>Recent research has discovered a connection between the AAA+ ATPase PSMC4 (Proteasome 26S Subunit, ATPase 4) and several forms of cancer. However, a detailed analysis of the oncogenic potential of PSMC4 was elusive. In this study, we anticipate PSMC4's potential as a cancer biomarker. We aimed to comprehensively assess the expression profiles, prognostic significance, and relevant cellular pathways associated with it. Through our examination of various types of cancers, PSMC4 is found to be overexpressed. Interestingly, our result finds a positive correlation between PSMC4 overexpression and unfavourable overall survival rates in cancer. Further, we looked into the mutations and copy number amplifications of PSMC4 across various cancers. Our study reveals that missense mutations plays a great role behind the oncogenic potential of PSMC4. Several possible mutation sites are predicted. Interestingly, we found fifteen hotspot mutations in the ATPase domain of PSMC4. Additionally, PSMC4 has shown a high amplification percentage in various cancers. We are additionally attentive to the functional characteristics of the protein PSMC4 across various types of cancer. In the protein-protein interaction analyses, it was found that multiple oncoproteins were directly interacting with PSMC4. The top signaling pathways of PSMC4 also indicate that it plays a crucial role in cancer development. Overall, this study reveals that PSMC4 could be a potential diagnostic and prognostic marker for cancer, making it a promising biomarker and target.</div></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"830 ","pages":"Article 111901"},"PeriodicalIF":1.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143464973","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}

{"title":"High expression of SLC34A2 contributes to chemoresistance of non-small cell lung cancer against gefitinib: The critical role of miR-124–3p","authors":"Chao Tan ,&nbsp;Li Zhang ,&nbsp;Sai Chen ,&nbsp;Zhenzhen Tian ,&nbsp;Nina Zhou ,&nbsp;Yuling Li ,&nbsp;Qi Wang ,&nbsp;Lu Chen","doi":"10.1016/j.mrfmmm.2024.111894","DOIUrl":"10.1016/j.mrfmmm.2024.111894","url":null,"abstract":"<div><div>Gefitinib is a therapeutic agent used to treat lung carcinoma, including non-small cell lung cancer (NSCLC). However, mechanisms underlying NSCLC cell resistance to gefitinib remain largely uncharacterized. In this study, we explored the association between the miR-124–3p/SLC34A2 axis and gefitinib resistance using a series of <em>in vivo</em> and <em>in vitro</em> assays. Data indicated that miR-124–3p is downregulated, while SLC34A2 is upregulated, in gefitinib-resistant NSCLC cells. Overexpression of miR-124–3p reduced NSCLC cell resistance to gefitinib by suppressing cell viability, inducing apoptosis, and decreasing N-cadherin expression. Conversely, inhibiting miR-124–3p in NSCLC cells led to increased cell viability and reduced apoptosis. Overexpression of SLC34A2 in NSCLC cells further heightened gefitinib resistance. In a xenograft mouse model, SLC34A2 overexpression promoted solid tumor growth and metastasis, while miR-124–3p overexpression inhibited these effects. Our results highlight that the interaction between miR-124–3p and SLC34A2 plays an indispensable role in determining gefitinib resistance in NSCLC cells.</div></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"830 ","pages":"Article 111894"},"PeriodicalIF":1.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696286","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}

{"title":"The mutagenic properties of formaldehyde and acetaldehyde: Reflections on half a century of progress","authors":"Mahanish Jung Thapa,&nbsp;Kin Chan","doi":"10.1016/j.mrfmmm.2024.111886","DOIUrl":"10.1016/j.mrfmmm.2024.111886","url":null,"abstract":"<div><div>Formaldehyde and acetaldehyde are reactive, small compounds that humans are exposed to routinely, variously from endogenous and exogenous sources. Both small aldehydes are classified as human carcinogens. Investigation of the DNA damaging properties of these two compounds began some 50 years ago. In this review, we summarize progress in this field since its inception over half a century ago, distilling insights gained by the collective efforts of many research groups while highlighting areas for future directions. Over the decades, general consensus about aspects of the mutagenicity of formaldehyde and acetaldehyde has been reached. But other characteristics of formaldehyde and acetaldehyde remain incompletely understood and require additional investigation. These include crucial details about the mutational signature(s) induced and possible mechanistic role(s) during carcinogenesis.</div></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"830 ","pages":"Article 111886"},"PeriodicalIF":1.5,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142645346","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}

{"title":"ATM and ATR gene editing mediated by CRISPR/Cas9 in Chinese Hamster cells","authors":"Junko Maeda,&nbsp;Piyawan Chailapakul,&nbsp;Takamitsu A. Kato","doi":"10.1016/j.mrfmmm.2024.111871","DOIUrl":"10.1016/j.mrfmmm.2024.111871","url":null,"abstract":"<div><p>Chinese hamster-derived cell lines including Chinese hamster lung fibroblasts (V79) have been used as model somatic cell lines in radiation biology and toxicology research for decades and have been instrumental in advancing our understanding of DNA damage response (DDR) mechanisms. Whereas many mutant lines deficient in DDR genes have been generated more than over decades, several key DDR genes such as ATM and ATR have not been established in the Chinese hamster system. Here, we transfected CRISPR/Cas9 vectors targeting Chinese hamster ATM or ATR into V79 cells and investigated whether the isolated clones had the characteristics reported in human and mouse studies. We obtained two clones of ATM knockout cells containing an insertion or deletions in the targeted locus. The ATM knockouts with no detectable ATM protein expression exhibited increased sensitivity to radiation and DNA double strand break inducing agents, cell cycle checkpoint defects and defective chromatid break repair. These are all characteristics of defective ATM function. Among the obtained ATR cells, which contained mutations in both ATR alleles while maintaining normal levels of ATR protein expression, one clone exhibited hypersensitivity to UV and replication stress agents. In the present study, we successfully established CRISPR-Cas9 derived ATM knockout cells. We couldn't knock out the ATR gene but obtained ATR mutant cells. Our results showed that Chinese hamster origin ATM knockout cells and ATR mutant cells could be useful tools for further research to reveal oncogenic functions and effects of developing anti-cancer therapeutics.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111871"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141638930","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}

{"title":"Understanding the nucleotide composition and patterns of codon usage in the expression of human oral cancer genes","authors":"Tarikul Huda Mazumder ,&nbsp;Arif Uddin","doi":"10.1016/j.mrfmmm.2024.111880","DOIUrl":"10.1016/j.mrfmmm.2024.111880","url":null,"abstract":"<div><p>Oral squamous cell carcinoma (OSCC) is primarily known as oral cancer (OC) that mostly occurs in mouth, lips and tongue. Mutations in some of the genes cause OC and some genes are risk factors for progression of OC. In this study, we analyzed the compositional features and pattern of codon usage in genes involved in OC using computational method as no work was reported yet. Compositional features suggested that the overall GC content was higher <em>i.e.</em> genes were GC rich. Effective number of codons (ENC) values ranged from 34.6 to 55.9 with a mean value of 49.03±4.22 representing low codon usage bias (CUB). Correspondence analysis (COA) suggested that the codon usage pattern was different in different genes. In genes associated with OC, highly significant correlation was observed between GC12 and GC3 (r=0.454, p&lt;0.01) suggesting that directional mutation affected all the three codon positions. This is the first report on pattern of codon usage pattern on genes involved in OC, which not only alludes a new perspective for elucidating the mechanisms of biased usage of synonymous codons but also provide valuable clues for molecular genetic engineering.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111880"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084355","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}

{"title":"Agrimonolide inhibits glycolysis in ovarian cancer cells by regulating HIF1A","authors":"Yi Yang,&nbsp;Huimin Wang,&nbsp;Qiong Wei,&nbsp;Chun Li","doi":"10.1016/j.mrfmmm.2024.111884","DOIUrl":"10.1016/j.mrfmmm.2024.111884","url":null,"abstract":"<div><h3>Background</h3><div>Ovarian cancer is one of the most common tumors affecting females, significantly disrupting their quality of life. Agrimonolide, an extract derived from Agrimony (<em>Agrimonia pilosa</em> Ledeb.), has been shown to exert various regulatory effects on several diseases. Notably, recent studies indicate that Agrimonolide may attenuate the progression of ovarian cancer. However, the detailed regulatory mechanisms of Agrimonolide in this context require further investigation.</div></div><div><h3>Purpose</h3><div>To determine the significance of HIF1A as a key target in ovarian cancer and its potential underlying signaling pathway.</div></div><div><h3>Methods</h3><div>Cell viability and proliferation were assessed using CCK-8 and colony formation assays. Glucose uptake and lactate production were measured using commercial kits, and the extracellular acidification rate (ECAR) was evaluated. Protein expression levels were analyzed through western blotting.</div></div><div><h3>Results</h3><div>Our network pharmacology analysis identified HIF1A as a crucial target and signaling pathway in ovarian cancer. Furthermore, treatment with Agrimonolide (20 μM and 40 μM) inhibited the growth of ovarian cancer cells. Agrimonolide also reduced glycolytic activity in these cells. Additionally, Agrimonolide treatment led to decreased expression levels of HIF1A, HK2, and LDHA in ovarian cancer cells. Rescue assays revealed that glucose uptake and lactate production were diminished following Agrimonolide treatment; however, these effects were reversed upon overexpression of HIF1A.</div></div><div><h3>Conclusion</h3><div>This study showed that Agrimonolide can suppress glycolysis in ovarian cancer cells by modulating HIF1A, supporting Agrimonolide as a promising therapeutic agent for ovarian cancer treatment.</div></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111884"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142357959","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}

{"title":"ALDH2 mutations and defense against genotoxic aldehydes in cancer and inherited bone marrow failure syndromes","authors":"Anthony Yiu-Ho Woo,&nbsp;Lina Jia","doi":"10.1016/j.mrfmmm.2024.111870","DOIUrl":"10.1016/j.mrfmmm.2024.111870","url":null,"abstract":"<div><p>Reactive aldehydes, for instance, formaldehyde and acetaldehyde, are important endogenous or environmental mutagens by virtue of their abilities to produce a DNA lesion called interstrand crosslink (ICL). Aldehyde-metabolizing enzymes such as aldehyde dehydrogenases (ALDHs) and the Fanconi anemia (FA) pathway constitute the main defense lines against aldehyde-induced genotoxicity. Biallelic mutations of genes in any one of the FA complementation groups can impair the ICL repair mechanism and cause FA, a heterogeneous disorder manifested by bone marrow failure (BMF), congenital abnormality and a strong predisposition to cancer. The defective <em>ALDH2</em> polymorphism rs671 (<em>ALDH2*2</em>) is a known risk and prognostic factor for alcohol drinking-associated cancers. Recent studies suggest that it also promotes BMF and cancer development in FA, and its combination with alcohol dehydrogenase 5 (ADH5) mutations causes aldehyde degradation deficiency syndrome (ADDS), also known by its symptoms as aplastic anemia, mental retardation, and dwarfism syndrome. <em>ALDH2*2</em> and another pathogenic variant in the alcohol-metabolizing pathway, <em>ADH1B1*1</em>, is prevalent among East Asians. Also, other <em>ALDH2</em> genotypes with disease-modifying potentials have lately been identified in different populations. Therefore, it would be appropriate to summarize current knowledge of genotoxic aldehydes and defense mechanisms against them to shed new light on the pathogenic effects of <em>ALDH2</em> variants together with other genetic and environmental modifiers on cancer and inherited BMF syndromes. Lastly, we also presented potential treatment strategies for FA, ADDS and cancer based on the manipulation of aldehyde-induced genotoxicity.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111870"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141474098","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}

{"title":"AQP5 promotes epithelial-mesenchymal transition and tumor growth through activating the Wnt/β-catenin pathway in triple-negative breast cancer","authors":"Zhengcai Zhu,&nbsp;Tao Li,&nbsp;Honggang Wang,&nbsp;Lianghe Jiao","doi":"10.1016/j.mrfmmm.2024.111868","DOIUrl":"10.1016/j.mrfmmm.2024.111868","url":null,"abstract":"<div><h3>Background</h3><p>Emerging data identifies aquaporin 5 (AQP5) as a vital player in many kinds of cancers. Over expression of AQP5 was associated with increased metastasis and poor prognosis, suggesting that AQP5 may facilitate cancer cell proliferation and migration. Our previous studies also showed that AQP3 and AQP5 were highly expressed in triple-negative breast cancer (TNBC) and the expression of AQP3 and AQP5 in TNBC tissue was positive correlated with advanced clinical stage.</p></div><div><h3>Objective</h3><p>We aim to investigate the role of AQP5 in TNBC oncogenesis and development.</p></div><div><h3>Methods</h3><p>MDA-MB-231 cells were transfected with siRNA-AQP5 and AQP5 overexpression vector to establish a differential expression system for AQP5. Cell proliferation and apoptosis of MDA-MB-231 cells were detected by CCK-8 (Cell Counting Kit-8) and FCM (flow cytometry), respectively. Cell migration and invasion abilities were evaluated by wound healing assay and transwell assay. The qRT-PCR and western blot assays were used to study the effect of AQP5 expression level on the expression of epithelial-to-mesenchymal transition (EMT) related molecules. The effects of ICG-001, a Wnt/β-catenin signaling pathway inhibitor, on the invasive and migratory capabilities of overexpressed AQP5 cells and downstream molecules were measured.</p></div><div><h3>Results</h3><p>1. The expression of AQP5 in the MDA-MB-231 cells was significantly higher than that in the MCF-10A cells. 2. Up-regulation of AQP5 significantly promoted the proliferation, migration and invasion of TNBC cells, while inhibited the cell apoptosis; in addition, up-regulation of AQP5 increased the expression of Bcl-2 and decreased the expression of Caspase-3. However, knockdown of AQP5 presented the adverse effects of AQP5 overexpression. 3. Overexpressed AQP5 induced the overexpression of EMT-related factors, which further promoted the migration and invasion of cells. 4. Overexpression of AQP5 could up-regulate the expression of β-catenin in the nucleus followed by increasing the expression levels of downstream genes in Wnt/β-catenin signaling pathway. Moreover, ICG-001, the inhibitor of Wnt/β-catenin signaling pathway, could significantly attenuate the effect of overexpression of AQP5 on cells, further confirming that AQP5 may promote the proliferation, migration and invasion of TNBC cells by activating Wnt/β-catenin signaling pathway.</p></div><div><h3>Conclusions</h3><p>In the TNBC cells, AQP5 modulates the expression levels of EMT-related proteins through activation of Wnt/β-catenin signaling pathway, thus enhancing the cell proliferation, migration and invasion while inhibiting the cell apoptosis.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111868"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141500041","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}

{"title":"HOXA1 promotes epithelial-mesenchymal transition and malignant characteristics of laryngeal squamous cell carcinoma","authors":"Jun Wu,&nbsp;Xiaofeng Gu","doi":"10.1016/j.mrfmmm.2024.111882","DOIUrl":"10.1016/j.mrfmmm.2024.111882","url":null,"abstract":"<div><p>Despite considerable advancements in the diagnosis and treatment of LSCC, there has been no significant improvement in survival rate. Consequently, identifying molecular targets for this cancer is of paramount importance. HOXA1, a constituent of the homeobox transcription factor cluster, plays a role in the development of various types of cancer. Nevertheless, the specific function and mechanism of HOXA1 in LSCC remains unclear. This study aimed to clarify the impact of HOXA1 on the advancement of LSCC and uncover its underlying mechanism. Our findings indicate that HOXA1 exhibits a significantly elevated expression level in LSCC. Suppression of HOXA1 inhibited the proliferation of LSCC cells. Furthermore, the ablation of HOXA1 triggered the apoptosis of LSCC cells and inhibited EMT. Functionally, HOXA1 has a role in initiating the activation of the PI3K/AKT/mTOR pathway in LSCC cells. In summary, HOXA1 significantly contributes to the EMT of LSCC cells via the PI3K/AKT/mTOR signaling pathway, thereby facilitating the proliferation and motility of LSCC cells. Consequently, HOXA1 presents itself as a viable therapeutic target for LSCC interventions.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111882"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142147240","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}

{"title":"The RAD51 S181P mutation shortens lifespan of female mice","authors":"Sherry G. Dodds ,&nbsp;Gene Hubbard ,&nbsp;Yong Jun Choi ,&nbsp;Kyungjae Myung ,&nbsp;Gene Elliot ,&nbsp;Lisa Garrett ,&nbsp;Tae Moon Kim ,&nbsp;Paul Hasty","doi":"10.1016/j.mrfmmm.2024.111878","DOIUrl":"10.1016/j.mrfmmm.2024.111878","url":null,"abstract":"<div><p>RAD51 is critical to the homologous recombination (HR) pathway that repairs DNA double strand breaks (DSBs) and protects replication forks (RFs). Previously, we showed that the S181P (SP) mutation in <em>RAD51</em> causes defective RF maintenance but is proficient for DSB repair. Here we report that SP/SP female mice exhibit a shortened lifespan compared to +/+ females but not males. Histological analysis found that most mice in this study died from lymphoma, independent of genotype and sex. We propose that a potential cause for shortened lifespan in SP/SP females is due to the RF defect.</p></div>","PeriodicalId":49790,"journal":{"name":"Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis","volume":"829 ","pages":"Article 111878"},"PeriodicalIF":1.5,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0027510724000289/pdfft?md5=39f47dbaabdae7ba92ee31eea49d1079&pid=1-s2.0-S0027510724000289-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141991132","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}