Cytojournal最新文献

{"title":"Development and validation of a multiparameter prognostic model for extranodal natural killer/T-cell lymphoma: Integration of clinical, pathological, and molecular biomarkers.","authors":"Shishou Wu, Yifei Liu, Lei Jiang, Licai An, Yuanfeng Zhang, Yu Pan, Liling Song, Yunjun Wang, Guohua Yu","doi":"10.25259/Cytojournal_34_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_34_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The objectives of the study are to develop and validate a novel prognostic model for extranodal natural killer/T-cell lymphoma (ENKTCL) by integrating clinical and pathological parameters.</p><p><strong>Material and methods: </strong>We retrospectively analyzed 106 patients with ENKTCL (2008-2020) from the Department of Pathology of Yantai Yuhuangding Hospital and the Affiliated Hospital of Nantong University, constructing the novel international prognostic index (NIPI) model through multivariable Cox regression of immunohistochemistry (IHC) markers (age, MTP53, Ki-67, lactate dehydrogenase, hemoglobin, platelet-tolymphocyte ratio) and quantitative dot blot (QDB) tumor microenvironment features.</p><p><strong>Results: </strong>The model demonstrated significant risk stratification (<i>P</i> < 0.001) with a 3-year area under the curve of 0.72 (IHC) and 0.80 (QDB), outperforming Ann Arbor staging (<i>P</i> > 0.05) and existing international prognostic index (<i>P</i> = 0.00036)/natural killer lymphoma prognostic index (<i>P</i> = 0.00017) models. The QDB-based implementation showed superior prognostic discrimination (<i>P</i> = 0.00014), highlighting its potential for precise individualized therapy.</p><p><strong>Conclusion: </strong>NIPI provides improved risk stratification for ENKTCL, and QDB-based analysis offers enhanced precision in individualized therapy. This model addresses the unmet needs for ENKTCL prognostication and warrants further multicenter validation.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"24"},"PeriodicalIF":3.1,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786352","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":"Topoisomerase II binding protein 1-interacting checkpoint and replication regulator promotes lung adenocarcinoma proliferation by regulating myelocytomatosis oncogene signaling pathway.","authors":"Yi Zhao, Yuan Feng, Mantao Guo, Linrui Li","doi":"10.25259/Cytojournal_24_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_24_2025","url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to investigate the role of topoisomerase II binding protein 1-interacting checkpoint and replication regulator (TICRR) on the proliferation of lung adenocarcinoma (LUAD) and its potential molecular mechanism as well as to provide a new strategy to improve LUAD treatment.</p><p><strong>Material and methods: </strong>The expression level of TICRR in patients with LUAD was analyzed on the basis of the Cancer Genome Atlas program database, and loss- and gain-of-function experiments were conducted to validate whether TICRR promoted the proliferation of LUAD cells. Then, pathway enrichment analysis and luciferase reporter assays were performed to dissect the potential mechanism.</p><p><strong>Results: </strong>Overexpression of TICRR in patients with LUAD was associated with poor survival (<i>P</i> < 0.001). In addition, overexpression of TICRR aggravated LUAD cell proliferation, which was ameliorated by TICRR depletion. In addition, TICRR could activate the myelocytomatosis oncogene (MYC) signaling pathway by regulating Bcl-2-associated X protein and Cyclin B1, which are the pivotal effectors of the MYC signaling pathway.</p><p><strong>Conclusion: </strong>TICRR plays a critical role in fostering the progression of LUAD by regulating the MYC signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"23"},"PeriodicalIF":3.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786763","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":"Cytology at the crossroads: Safeguarding equity in the molecular era.","authors":"Cristina Díaz Del Arco","doi":"10.25259/Cytojournal_203_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_203_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"22"},"PeriodicalIF":3.1,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786308","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":"Mapping the function of EF-hand domain-containing protein 2 and determining its clinical relevance in non-small-cell lung cancer through single-cell transcriptomics.","authors":"Xueping Luo, Feng Zhang, Zhiyu Li, Chucheng Zhong, Xiaozhen Shen","doi":"10.25259/Cytojournal_29_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_29_2025","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the cellular composition and transcriptional variability within the tumor microenvironment (TME) of non-small-cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNAseq) and to assess the role of EF-hand domain-containing protein 2 (EFHD2) in tumor progression and its involvement in relevant signaling pathways.</p><p><strong>Material and methods: </strong>We analyzed scRNA-seq datasets to map the cellular and transcriptional landscape of NSCLC tumors. Immunohistochemistry (IHC) was employed to validate the expression of EFHD2 and assess immune cell infiltration in clinical samples. To further investigate the functional effect of EFHD2, we performed Western blot and quantitative real-time polymerase chain reaction analyses as well as cell proliferation, migration, invasion, and apoptosis assays. We also explored the janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathway as a potential underlying mechanism.</p><p><strong>Results: </strong>The scRNA-seq analysis revealed that epithelial cells were the predominant population within the TME, alongside endothelial cells, fibroblasts, macrophages, and a small proportion of stem cells. EFHD2 expression exhibited considerable variability, with higher levels associated with clusters enriched in transcriptionally active and immunomodulatory pathways. The IHC results demonstrated elevated EFHD2 expression and immune cell infiltration in tumor tissues compared with adjacent non-tumor tissues.</p><p><strong>Conclusion: </strong>EFHD2 expression in the NSCLC TME correlates with immune cell infiltration and may play a significant role in tumor progression and immune modulation. The JAK-STAT signaling pathway may be a potential mechanism underlying the effect of EFHD2. This work provides a new avenue for targeted therapy in NSCLC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"21"},"PeriodicalIF":3.1,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786803","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":"Ubiquitin-specific protease 5 promotes breast cancer progression by stabilizing Forkhead box M1 through deubiquitination.","authors":"Xiaoyan Wang, Tingting Chen, Songsong Wu, Youyi Wu","doi":"10.25259/Cytojournal_39_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_39_2025","url":null,"abstract":"<p><strong>Objective: </strong>Breast cancer continues to be a leading and aggressive cancer in women. Despite improvements in early treatment, challenges such as rapid tumor proliferation, metastasis, and drug resistance persist. This research examines how the deubiquitinase ubiquitin-specific protease 5 (USP5) maintains Forkhead box M1 (FOXM1) protein stability and its impact on the advancement of breast cancer.</p><p><strong>Material and methods: </strong>Data from The Cancer Genome Atlas were utilized to investigate the expression patterns and interactions of USP5 and FOXM1 in breast cancer. The breast cancer cell lines were subjected to functional testing, including invasion, migration, and proliferation. The expression and interaction of USP5 and FOXM1 were examined using quantitative real-time polymerase chain reaction, Western blot, and co-immunoprecipitation analyses. Protein stability and ubiquitination assays were performed to evaluate the effect of USP5 on FOXM1 stability.</p><p><strong>Results: </strong>USP5 stabilized the FOXM1 protein by deubiquitination. Overexpression of USP5 increased FOXM1 levels, while USP5 knockdown accelerated FOXM1 degradation. The deubiquitinating enzyme USP5 inhibited the proteasomal degradation of FOXM1, enhancing its stability. Functional assays showed that USP5 overexpression promoted breast cancer cell progression, while USP5 knockdown inhibited these malignant phenotypes. <i>In vivo</i> analysis showed that FOXM1 knockdown reduced tumor volume, and USP5 overexpression with FOXM1 knockdown increased tumor size. The findings suggest that USP5 promotes breast cancer progression by regulating FOXM1 stability.</p><p><strong>Conclusion: </strong>USP5 enhances breast cancer progression by stabilizing FOXM1 through deubiquitination.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"18"},"PeriodicalIF":3.1,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786825","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":"Diagnostic accuracy of the Yokohama system for reporting breast fine-needle aspiration cytology and breast imaging-reporting and data system in breast lesions.","authors":"Shakthivel V, Sana Ahuja, Sufian Zaheer, Swarna Swarna, Mukul Singh, Chintamani Chintamani","doi":"10.25259/Cytojournal_167_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_167_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The Yokohama system standardizes fine-needle aspiration cytology (FNAC) reporting for breast lesions, while the breast imaging-reporting and data system (BI-RADS) categorizes lesions based on imaging risk assessment. This study aimed to evaluate the diagnostic accuracy of FNAC using the Yokohama System in correlation with BI-RADS classifications.</p><p><strong>Material and methods: </strong>A retrospective analysis was conducted on 188 breast lesion cases that underwent FNAC and were categorized using the BI-RADS system. The breast FNAs were classified according to the Yokohama System and compared with histopathological diagnoses to calculate the risk of malignancy (ROM). The ROM for the BI-RADS categories was also determined. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for both.</p><p><strong>Results: </strong>According to the Yokohama classification, 5.9%, 52.1%, 4.8%, 8.5%, and 28.7% were classified as non-diagnostic, benign, atypical, suspicious, and malignant, respectively. The majority of cases were classified as BIRADS 3 (23.9%) and 5 (23.9%), followed by 4a (22.3%). Higher Yokohama and BI-RADS categories were more prevalent among malignant cases, with 64.9% in Yokohama category 5 and 51.9% in BI-RADS 5. Sensitivity was highest in Yokohama Scenario C (81.8%), while specificity (96.4%) and PPV (92.6%) were highest in Scenario A. When BI-RADS 4b, 4c, 5, and 6 were considered malignant, Scenario C had the highest sensitivity (87.0%) and NPV (90.4%), while Scenario B demonstrated the highest diagnostic accuracy (87.7%).</p><p><strong>Conclusion: </strong>FNAC using the Yokohama System and imaging-based BI-RADS classification both show high diagnostic accuracy for breast lesions. While their individual performance is comparable, further studies are needed to explore whether combining these modalities improves diagnostic outcomes in clinically indeterminate cases.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"20"},"PeriodicalIF":3.1,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786832","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":"BDNF facilitates ectopic endometrial stromal cell growth, invasion, migration and glycolysis in endometriosis via upregulating GLUT1.","authors":"Yapeng Han, Yang Yu, Yaguang Han, Wei Guan, Jieming Li, Boyi Feng, Chang Sun, Hong Ying Kuang","doi":"10.25259/Cytojournal_169_2024","DOIUrl":"https://doi.org/10.25259/Cytojournal_169_2024","url":null,"abstract":"<p><strong>Objective: </strong>Brain-derived neurotrophic factor (BDNF) is considered to participate in regulating the endometriosis (EM) process. However, other functions and mechanisms of BDNF in EM progression still need to be further studied.</p><p><strong>Material and methods: </strong>Ectopic/normal endometrial stromal cells (ESCs) were isolated from EM tissues/normal control endometrial tissues. BDNF mRNA expression in EM tissues and normal control endometrial tissues was analyzed through quantitative real-time polymerase chain reaction. The protein levels of BDNF and glucose transporter 1 (GLUT1) were detected by Western blot. The function of ESCs was determined through cell counting kit 8 assay, 5-ethynyl-2'-deoxyuridine assay, flow cytometry, Transwell assay, and wound healing assay. The interaction between BDNF and GLUT1 was assessed through a co-immunoprecipitation assay and immunofluorescence staining.</p><p><strong>Results: </strong>BDNF expression was elevated in EM tissues and ectopic ESCs. Functional experiments revealed that BDNF knockdown repressed ectopic ESC proliferation, invasion, migration, and glycolysis and promoted apoptosis. In terms of mechanism, BDNF interacted with GLUT1 to enhance its protein expression. In addition, the repressing effect of BDNF knockdown on ectopic ESCs' growth, invasion, migration, and glycolysis was abolished by GLUT1 overexpression.</p><p><strong>Conclusion: </strong>Our study showed that BDNF could facilitate ectopic ESC function by interacting with GLUT1, thereby providing basic information for finding an effective therapeutic target of EM.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"19"},"PeriodicalIF":3.1,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786996","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":"Destaining hematoxylin and eosin stains and restaining for immunohistochemistry has diagnostic value for cytology samples.","authors":"Mohammad M Al-Attar, Tianle Zou, Salwa Khedr, Min Zhang, Karen Dresser, Andrew H Fischer","doi":"10.25259/Cytojournal_171_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_171_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The use of one antibody per slide for immunohistochemical (IHC) studies is difficult to interpret when neoplastic cells are sparse, mixed with complex mixtures of other cells, or are obscured by the IHC stain itself. To accurately assign IHC results to particular neoplastic cells, we developed and validated a technique of destaining hematoxylin and eosin (H&E) stains and restaining (DSRS) by IHC on cytology cell block sections and studied its utility.</p><p><strong>Materials and methods: </strong>We identified 9 patients with fine needle aspiration (FNA) samples performed for a variety of tumors. Specimens were collected and made into ThinPreps and cell blocks. Cell block serial H&E stains revealed a rich background of benign cells, with rare scattered atypical cells arranged singly or in small clusters. Select H&E slides were scanned, destained, and then restained with one IHC biomarker per H&E. Slide scanning and image synchronization were used in tracking neoplastic cells. IHC results were validated for the DSRS process for all antibodies without the need for modification of the IHC protocol. Diagnoses rendered on the limited FNA samples were compared with those made on core biopsies, resections, or cytologic samples with ample cell quantity.</p><p><strong>Results: </strong>DSRS of the limited FNA samples did not compromise the quality of tissues or IHC, and comparison of the limited FNA diagnosis and final diagnosis rendered on more adequate specimens revealed concordant and accurate diagnosis in 89% (8/9) of cases, in contrast to a concordance rate of 22% (2/9) before the use of DSRS while the immunostain interpretation accuracy rate is 100% (9/9).</p><p><strong>Conclusion: </strong>DSRS of cytology cell block sections allows IHC stains to be ascribed to particular cells, enabling diagnosis when material is sparse, when diagnostic cells are admixed with other cell types, and when the IHC stain itself would otherwise obscure the identity of cells. DSRS provides an inexpensive alternative to other, more advanced techniques such as multiplex IHC or immunofluorescence.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"17"},"PeriodicalIF":3.1,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786315","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":"SA4503 plays a protective role in post-resuscitation injury by reducing apoptosis caused by mitochondrial dysfunction and endoplasmic reticulum stress through the activation of sigma-1 receptor.","authors":"Yijie Wang, Yi Li, Haiyan Zhao, Rong Liu, Jilin Yang, Ting Li, Chen He, Jiahong Qin","doi":"10.25259/Cytojournal_55_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_55_2025","url":null,"abstract":"<p><strong>Objective: </strong>Cardiac arrest followed by resuscitation can induce brain injury, and currently, there are no effective treatments for brain damage after cardiopulmonary resuscitation (CPR), necessitating the exploration of additional therapeutic strategies and prevention approaches. This study aimed to investigate the mechanism of action by which SA4503 activates the Sigma-1 receptor (Sig-1R) to protect against ischemic brain injury in both <i>in vitro</i> and <i>in vivo</i> models. The goal of this study was to provide theoretical support for SA4503 as a potential therapeutic agent and promote clinical intervention research for post-resuscitation brain injury following CPR.</p><p><strong>Material and methods: </strong>This study explored the mechanism underlying the ability of Sig-1R activation to mitigate brain injury following cardiac arrest and resuscitation in rats through both <i>in vivo</i> and <i>in vitro</i> models. The methods used include enzyme-linked immunosorbent assay, magnetic resonance imaging, Western blot analysis, and flow cytometry.</p><p><strong>Results: </strong>The <i>in vivo</i> results demonstrated that the Sig-1R agonist SA4503 significantly attenuated neurological deficits in rats subjected to CPR. <i>In vitro</i> mechanistic investigations revealed that SA4503 potently reversed Sig-1R protein downregulation, reduced apoptosis, ameliorated mitochondrial dysfunction, and reduced endoplasmic reticulum (ER) stress in the oxygen-glucose deprivation/reperfusion (OGD/R) group.</p><p><strong>Conclusion: </strong>This study further confirms that Sig-1R activation confers protective effects against brain injury following cardiac arrest and resuscitation, as well as against OGD/R-induced injury in HT22 cells. The underlying mechanism involves the mitigation of apoptosis driven by mitochondrial dysfunction and ER stress.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"16"},"PeriodicalIF":3.1,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786837","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":"Koilocytes in the era of molecular viral detection: Still a useful cytopathic effect of human papillomavirus?","authors":"Haissa O Brito, Leonardo Maciel, Rui Miguel Gil da Costa","doi":"10.25259/Cytojournal_168_2025","DOIUrl":"https://doi.org/10.25259/Cytojournal_168_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"14"},"PeriodicalIF":3.1,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786791","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}