Molecular medicine reports最新文献

{"title":"Expression of the IGF‑1Ea isoform in human placentas from third trimester normal and idiopathic intrauterine growth restriction singleton pregnancies: Correlations with clinical and histopathological parameters.","authors":"Apostolos Fasoulopoulos, Michail Varras, Fani-Niki Varra, Anastasios Philippou, Despina Myoteri, Viktoria-Konstantina Varra, Evgenia Kouroglou, Alexandros Gryparis, Argyro Papadopetraki, Iakovos Vlachos, Konstantinos Papadopoulos, Michael Koutsilieris, Anastasia Evangelia Konstantinidou","doi":"10.3892/mmr.2025.13434","DOIUrl":"10.3892/mmr.2025.13434","url":null,"abstract":"<p><p>Intrauterine growth restriction (IUGR) is the second most common obstetric complication after preterm labor. Appropriate trophoblast differentiation and placental structure, growth and function are key for the maintenance of pregnancy and normal fetal growth, development and survival. Extravillous trophoblast cell proliferation, migration and invasion are regulated by molecules produced by the fetomaternal interface, including autocrine factors produced by the trophoblast, such as insulin‑like growth factor (IGF)‑1. The aim of the present study was to investigate expression patterns of IGF‑1Ea isoform in IUGR placenta compared with appropriate for gestational age (AGA) pregnancies. Placental frozen tissues were collected from 13 AGA and 15 IUGR third trimester pregnancies for detection of IGF‑1Ea mRNA expression using reverse transcription‑quantitative PCR. Formalin‑fixed paraffin‑embedded samples from 15 AGA and 47 IUGR pregnancies were analyzed immunohistochemically for the identification and localization of the IGF‑1Ea peptide and comparison of clinical and histopathological parameters. To the best of our knowledge, the present study is the first to show IGF‑1Ea expression in third trimester human placenta. The results indicated that similar IGF‑1Ea mRNA expression levels were present in placental specimens from both groups. Cytoplasmic IGF‑1Ea expression was localized in the perivillous syncytiotrophoblast, extravillous trophoblast and endothelium of the villous and decidual vessels in both groups. No significant difference in the scores and intensity of IGF‑1Ea expression in perivillous syncytiotrophoblasts were noted in the IUGR vs. AGA pregnancies. Most IUGR cases showed negative IGF‑1Ea expression in the extravillous trophoblast, whereas AGA pregnancies showed predominantly positive immunostaining. A sex‑specific expression pattern was noted in the extravillous trophoblast, with negative IGF‑1Ea expression in the placentas of female IUGR cases. Additionally, positive immunostaining for IGF‑1Ea peptide in fetal villous and maternal decidual vessels, was more frequently observed in the IUGR group compared with AGA. In conclusion, no difference in total IGF‑1Ea mRNA placental expression was observed between IUGR and AGA pregnancies, likely due to heterogeneity of histological structures expressing this isoform. Negative IGF‑1Ea immunohistological expression in the extravillous trophoblast from IUGR placentas, associated with histological changes of maternal malperfusion, may reflect the involvement of this isoform in defective placentation. The presence of IGF‑1Ea peptide in the endothelium of the villous vessels in IUGR placentas may indicate a reactive autocrine regulation to compensate for malperfused villi in IUGR pregnancy by regulating angiogenesis and vasodilation. The observed sex differences in IGF‑1Ea expression between IUGR and AGA placentas may indicate interactions between sex hormones and selective IGF‑1 binding proteins ","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751665/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951891","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}

{"title":"[Retracted] NG25, an inhibitor of transforming growth factor‑β‑activated kinase 1, ameliorates neuronal apoptosis in neonatal hypoxic‑ischemic rats.","authors":"Hua Wang, Zhong Chen, Yu Li, Qiaoyun Ji","doi":"10.3892/mmr.2024.13423","DOIUrl":"10.3892/mmr.2024.13423","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the TUNEL assay data shown in Fig. 4B were strikingly similar to data appearing in different form in another article written by different authors at different research institutes that had already been submitted for publication to the journal <i>Experimental and Therapeutic Medicine</i> (which has subsequently been retracted). Owing to the fact that these contentious data had already apparently been submitted for publication prior to the receipt of this paper to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 1710-1716, 2018; DOI: 10.3892/mmr.2017.8024].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11715618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882555","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}

{"title":"New insights into the role of complement system in colorectal cancer (Review).","authors":"Yuwen Xu, Jiaqi Zhou, Yuanyuan Wu, Jie Shen, Xiaoyan Fu, Meifang Liu, Shujuan Liang","doi":"10.3892/mmr.2025.13433","DOIUrl":"10.3892/mmr.2025.13433","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the most common cancers worldwide. With the growing understanding of immune regulation in tumors, the complement system has been recognized as a key regulator of tumor immunity. Traditionally, the complement cascade, considered an evolutionarily conserved defense mechanism against invading pathogens, has been viewed as a crucial inhibitor of tumor progression. Complement components or activation products produced via cascade‑dependent or ‑independent processes are associated with the regulation of tumor‑associated inflammation. Various forms of complement activation products present in body fluids or inside cells, along with complement regulatory proteins and complement receptors, are involved in tumor cell growth and modulating the tumor microenvironment. In the present review, the role of the complement system in the tumor immunity of CRC is discussed. In addition, the contribution of the unconventional cascade‑independent pathway of complement activation in CRC progression is highlighted. A deeper understanding of the mechanism underlying the complement system in colitis‑associated colorectal cancer (CAC) may provide novel insights to assist the development of methods to prevent tumor progression and identify potential targets for the treatment of CAC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951896","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}

{"title":"Insights into renal damage in hyperuricemia: Focus on renal protection (Review).","authors":"Hang Yang, Jie Ying, Tong Zu, Xiao-Ming Meng, Juan Jin","doi":"10.3892/mmr.2024.13424","DOIUrl":"10.3892/mmr.2024.13424","url":null,"abstract":"<p><p>The incidence of hyperuricemia has increased recently, posing a serious threat to public health. Hyperuricemia is associated with an increased risk of gout, chronic kidney disease (CKD), obesity, metabolic syndrome, type 2 diabetes mellitus, hypertension, hypertriglyceridaemia, metabolic dysfunction‑associated steatotic liver disease, acute kidney injury, coronary heart disease and cardiovascular disease (CVD). These diseases are commonly accompanied by varying degrees of kidney damage. A number of randomized controlled clinical trials have investigated the effectiveness of UA‑lowering therapies in preventing kidney disease progression. The present review provided fundamental insights into the pathogenesis, principles and therapeutic approaches for managing hyperuricemia in patients with aforementioned diseases and assesses the effect of uric acid‑lowering therapy on diabetic nephropathy, systemic lupus erythematosus, CKD, CVD and obesity progression.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11711934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142882559","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}

{"title":"Epigenetic downregulation of the proapoptotic gene <i>HOXA5</i> in oral squamous cell carcinoma.","authors":"Ying-Ju Chen, Shin-Wei Liao, Yen-Ling Lai, Yu-Fen Li, Yin-Che Lu, Chien-Kuo Tai","doi":"10.3892/mmr.2024.13421","DOIUrl":"10.3892/mmr.2024.13421","url":null,"abstract":"<p><p>Homeobox A5 (<i>HOXA5</i>) has been identified as a tumor suppressor gene in breast cancers, but its role in oral squamous cell carcinoma (OSCC) has not been confirmed. The Illumina GoldenGate Assay for methylation identified that DNA methylation patterns differ between tumorous and normal tissues in the oral cavity and that <i>HOXA5</i> is one of the genes that are hypermethylated in oral tumor tissues. The present study obtained more‑complete information on the methylation status of <i>HOXA5</i> by using the Illumina Infinium MethylationEPIC BeadChip and bisulfite sequencing assays. The results indicated that <i>HOXA5</i> hypermethylation has great potential as a biomarker for detecting OSCC. Comparing <i>HOXA5</i> RNA expression between normal oral tissue and OSCC tissue samples indicated that its median level was 2.06‑fold higher in normal tissues that in OSCC tissues. Moreover, treatment using the demethylating agent 5‑aza‑2'‑deoxycytidine can upregulate <i>HOXA5</i> expression in OSCC cell lines, verifying that the silencing of <i>HOXA5</i> is primarily regulated by its hypermethylation. It was also found that upregulation of <i>HOXA5</i> expression can not only increase OSCC cell death but that it can also enhance the therapeutic effect of cisplatin both <i>in vitro</i> and <i>in vivo</i>, suggesting that <i>HOXA5</i> is an epigenetically downregulated proapoptotic gene in OSCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864062","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}

{"title":"Pin1 as a central node in oncogenic signaling: Mechanistic insights and clinical prospects (Review).","authors":"Shuning Lei, Min Luo, Yuxue Wang","doi":"10.3892/mmr.2025.13445","DOIUrl":"10.3892/mmr.2025.13445","url":null,"abstract":"<p><p>Peptidyl‑prolyl cis‑trans isomerase NIMA-interacting 1 (Pin1) is a specific phosphorylated serine/threonine-proline cis-trans isomerase, which is involved in the regulation of a variety of physiological and pathological processes, including cell cycle progression, proliferation and apoptosis. Pin1 plays a key role in tumorigenesis and tumor development and it promotes the proliferation and metastasis of cancer cells by regulating the cell cycle, signaling pathways and the function of tumor suppressors. Upregulated expression of Pin1 is closely associated with a poor prognosis in several types of cancers. Thus, Pin1 is may have potential as a novel potential biomarker for tumor diagnosis and prognosis, as well as a promising anticancer target. The aim of the present review was to discuss the mechanism of Pin1 in tumors and recent research progress in this field.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066695","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}

{"title":"Mitochondrial DNA copy number alterations: Key players in the complexity of glioblastoma (Review).","authors":"Abdul Aziz Mohamed Yusoff, Siti Zulaikha Nashwa Mohd Khair, Siti Muslihah Abd Radzak","doi":"10.3892/mmr.2025.13443","DOIUrl":"10.3892/mmr.2025.13443","url":null,"abstract":"<p><p>Renowned as a highly invasive and lethal tumor derived from neural stem cells in the central nervous system, glioblastoma (GBM) exhibits substantial histopathological variation and genomic complexity, which drive its rapid progression and therapeutic resistance. Alterations in mitochondrial DNA (mtDNA) copy number (CN) serve a crucial role in GBM development and progression, affecting various aspects of tumor biology, including energy production, oxidative stress regulation and cellular adaptability. Fluctuations in mtDNA levels, whether elevated or diminished, can impair mitochondrial function, potentially disrupting oxidative phosphorylation and amplifying reactive oxygen species generation, thereby fueling tumor growth and influencing treatment responses. Understanding the mechanisms of mtDNA‑CN variations, and their interplay with genetic and environmental elements in the tumor microenvironment, is essential for advancing diagnostic and therapeutic strategies. Targeting mtDNA alterations could strengthen treatment efficacy, mitigate resistance and ultimately enhance the prognosis of patients with this aggressive brain tumor. The present review summarizes the existing literature on mtDNA alterations, specifically emphasizing variations in mtDNA‑CN and their association with GBM by surveying articles published between 1996 and 2024, sourced from databases such as Scopus, PubMed and Google Scholar. In addition, the review provides a brief overview of mitochondrial genome architecture, knowledge regarding the regulation of mtDNA integrity and CN, and how mitochondria significantly impact GBM tumorigenesis. This review further presents information on therapeutic approaches for restoring mtDNA‑CN that contribute to optimized mitochondrial function and improved health outcomes.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11795256/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143066771","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}

{"title":"[Retracted] Limb remote ischemic post‑conditioning reduces injury and improves long‑term behavioral recovery in rats following subarachnoid hemorrhage: Possible involvement of the autophagic process.","authors":"Xiang Hu, Tao Lv, Shao-Feng Yang, Xiao-Hua Zhang, Yi-Feng Miao","doi":"10.3892/mmr.2024.13419","DOIUrl":"10.3892/mmr.2024.13419","url":null,"abstract":"<p><p>Following the publication of the above paper, a concerned reader drew to the attention of the Editorial Office that the 'Sham' brain image featured in Fig. 1B on p. 23 was strikingly similar to an image that was published subsequently in the journal <i>Scientific Reports</i>, whereas the control TUNEL assay data shown in Fig. 4A on p. 25 were similarly strikingly similar to data shown in a paper published previously in the journal <i>Mediators of Inflammation</i>, even though the overall experiments portrayed in the other journals were different. As the three affected articles did hold at least one author in common, we asked the authors to provide an explanation to account for the sharing of these data among these papers, but no reply was forthcoming from them; therefore, in the absence of a reply from these authors, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 21‑30, 2018; DOI: 10.3892/mmr.2017.7858].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683449/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864060","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}

{"title":"NEDD4 enhances bone‑tendon healing in rotator cuff tears by reducing fatty infiltration.","authors":"Jian Li, Ying Peng, Dong Zhen, Caifen Guo, Wuxun Peng","doi":"10.3892/mmr.2024.13420","DOIUrl":"10.3892/mmr.2024.13420","url":null,"abstract":"<p><p>Rotator cuff tears (RCT) can cause shoulder pain, weakness and stiffness, significantly affecting daily life. Analysis of the GSE103266 dataset revealed significant changes in the mTOR/PI3K/Akt signaling pathway and lipid metabolism‑related pathways, suggesting that fatty infiltration may affect RCT. The analysis indicated that the ubiquitin ligase NEDD4 plays a critical role in RCT. NEDD4 was found to be highly associated with the mTOR/PI3K/Akt signaling pathway. An RCT model in Sprague‑Dawley (SD) rats was established to study the role of NEDD4 in regulating the mTOR pathway and investigate its effects on fatty infiltration. SD rats were divided into NEDD4 overexpression and knockout groups. Tissue recovery, apoptosis and fat deposition were measured through histological staining, reverse transcription‑quantitative PCR and western blotting. Additionally, cell culture of fibro‑adipogenic progenitors and lentiviral transfection were conducted to investigate the effect of NEDD4 on adipocyte differentiation. NEDD4 overexpression significantly reduced lipid accumulation, whereas NEDD4 knockdown enhanced lipid accumulation. NEDD4 was found to regulate the mTOR pathway and the expression of adipogenesis‑related genes, promoting fat metabolism and inhibiting adipocyte differentiation. Histological analysis indicated that NEDD4 overexpression improved tissue recovery and reduced apoptosis. Targeting NEDD4 offers a potential therapeutic strategy to improve the clinical outcomes of patients with RCT by modulating the mTOR pathway and fat metabolism.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864073","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}

{"title":"Calycosin‑7‑O‑β‑D‑glucoside downregulates mitophagy by mitigating mitochondrial fission to protect HT22 cells from oxygen‑glucose deprivation/reperfusion‑induced injury.","authors":"Xiangli Yan, Siqi Quan, Roujia Guo, Zibo Li, Ming Bai, Baoying Wang, Pan Su, Erping Xu, Yucheng Li","doi":"10.3892/mmr.2025.13436","DOIUrl":"10.3892/mmr.2025.13436","url":null,"abstract":"<p><p>Calycosin‑7‑O‑β‑D‑glucoside (CG), a major active ingredient of Astragali Radix, exerts neuroprotective effects against cerebral ischemia; however, whether the effects of CG are associated with mitochondrial protection remains unclear. The present study explored the role of CG in improving mitochondrial function in a HT22 cell model of oxygen‑glucose deprivation/reperfusion (OGD/R). The Cell Counting Kit‑8 assay, flow cytometry, immunofluorescence and western blotting were performed to investigate the effects of CG on mitochondrial function. The results demonstrated that mitochondrial function was restored after treatment with CG, as indicated by reduced mitochondrial reactive oxygen species levels, increased mitochondrial membrane potential and improved mitochondrial morphology. Overactivated mitophagy was revealed to be inhibited by the regulation of proteins involved in fission [phosphorylated‑dynamin‑related protein 1 (Drp1) and Drp1] and mitophagy (LC3, p62 and translocase of outer mitochondrial membrane 20), and mitochondrial biogenesis was demonstrated to be enhanced by increased levels of sirtuin 1 (SIRT1) and peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α). In addition, neuronal apoptosis was ameliorated by CG, as determined by a decreased rate of apoptosis, and levels of caspase‑3 and Bcl‑2/Bax. In conclusion, the present study demonstrated that CG may alleviate OGD/R‑induced injury by upregulating SIRT1 and PGC‑1α protein expression, and reducing excessive mitochondrial fission and overactivation of mitophagy.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008524","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}