Pathology, research and practice最新文献

{"title":"Biomarker-guided targeted therapy in lung adenocarcinoma: A concise review of precision oncology advances, resistance mechanisms, and emerging strategies.","authors":"Tanisqa Mall, Vishwajeet Bachhar, Vibha Joshi, Meng-Chih Lin, Chien-Hsing Wu, Chung-Hsien Hung, Chiung-I Tsai, Guo-Ping Chang-Chien, Sakthivel Kogularasu","doi":"10.1016/j.prp.2026.156711","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156711","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD), a major subtype of non-small cell lung cancer (NSCLC), remains a leading cause of cancer-related mortality despite major therapeutic advances. Precision oncology has revolutionized the management of LUAD by identifying actionable molecular biomarkers and developing targeted therapies. In this review, we summarize the major predictive biomarkers in LUAD, including EGFR, KRAS, ALK, ROS1, MET, RET, BRAF, HER2, NTRK, and PD-L1, and describe the currently approved targeted therapies and emerging therapeutic strategies. Recent advances in selective inhibitors, antibody-drug conjugates, and immune checkpoint inhibitors that have improved clinical outcomes in molecularly defined patient populations are highlighted. The review also discusses the molecular basis of acquired resistance, such as on-target mutations, bypass signalling activation, histological transformation, and epithelial-mesenchymal transition that continue to limit long-term therapeutic efficacy. We also discuss emerging strategies to overcome resistance, including combination therapies, next-generation inhibitors, liquid biopsy-guided monitoring, and artificial intelligence-assisted precision medicine. Collectively, these findings highlight the need for comprehensive molecular characterization and integrated biomarker-guided treatment strategies to improve therapeutic decision-making and clinical outcomes in LUAD.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156711"},"PeriodicalIF":3.7,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149245539","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":"Sperm telomere length: A potential reflection of genomic integrity and environmental influences on male fertility.","authors":"Hojat Ghasemnejad-Berenji, Ali Parvin, Mahdi Farasati, Muhammad Attar, Ramtin Naderian, Keivan Lashkari, Mortaza Taheri-Anganeh","doi":"10.1016/j.prp.2026.156709","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156709","url":null,"abstract":"<p><p>Infertility affects nearly one in six people worldwide, with male-related factors contributing to approximately half of all cases. Although conventional semen analysis remains central to the assessment of male fertility, it provides limited insight into sperm genomic competence and has only modest value for predicting reproductive outcomes. Sperm telomere length (STL) has therefore gained attention as a potential marker of germ-cell history, genomic integrity, and cumulative exposure to environmental and metabolic stress. Evidence from human studies, however, remains inconsistent. Associations between STL, conventional semen parameters, and assisted reproductive technology (ART) outcomes vary across studies, likely because of differences in study populations, sperm preparation and purification methods, somatic-cell contamination, sample size, confounder adjustment, outcome definitions, and analytical platforms. Among the most widely used methods, quantitative polymerase chain reaction (qPCR) provides a relative estimate of mean telomere length based on the telomere-to-single-copy-gene (T/S) ratio in bulk samples, whereas quantitative fluorescence in situ hybridization (qFISH) enables assessment of telomere-signal distributions at the single-cell level. Both approaches offer distinct advantages and limitations, and neither has demonstrated clear clinical superiority. This review integrates current biological, methodological, environmental, and clinical evidence and proposes a cautious mechanistic framework linking oxidative stress, mitochondrial dysfunction, telomeric DNA damage, chromatin organization, STL variation, and reproductive outcomes. While STL is biologically plausible as an investigational marker of sperm quality, current evidence is insufficient to support its routine clinical use. Larger, standardized, and well-controlled studies are needed to establish whether STL provides meaningful information beyond existing measures of male fertility.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156709"},"PeriodicalIF":3.7,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224783","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":"Quercetin in oral squamous cell carcinoma: Integrating immunometabolic reprogramming, cancer stem cell plasticity, and precision therapeutic strategies.","authors":"Rohit Das, Shikha Yadav, Sudeshna Das, Shatrudhan Prajapati","doi":"10.1016/j.prp.2026.156710","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156710","url":null,"abstract":"<p><p>Oral squamous cell carcinoma (OSCC) remains a major clinical challenge because of its recurrence, metastasis, and therapeutic resistance. Quercetin, a dietary flavonoid, has shown broad anticancer activity in experimental models of OSCC through the modulation of several processes, including apoptosis, autophagy, oxidative stress, epithelial-mesenchymal transition (EMT), cancer stem cell (CSC) phenotypes, metabolism, inflammation, and oncogenic signalling. However, the available evidence remains largely preclinical, and no clinical trial has demonstrated an improvement in progression-free survival or overall survival with quercetin in OSCC. Limited tumour exposure, poor predictability of pharmacokinetic behaviour, and the absence of validated predictive biomarkers further restrict its clinical translation. This review therefore moves beyond a pathway-based description of quercetin activity and discusses its potential within a biomarker-guided and translational framework. The roles of patient-derived organoids (PDOs), molecular profiling, and multi-omics approaches in identifying OSCC subgroups that may be sensitive to quercetin and in understanding response and resistance mechanisms are explored. In addition, artificial intelligence (AI)-assisted approaches are considered for the rational prioritization of combination therapies, integration of molecular and pharmacological data, and optimization of patient selection. We propose a stepwise development strategy involving PDO-guided studies, pharmacokinetic optimization, biomarker-enriched early-phase trials, and subsequent evaluation of clinically meaningful outcomes in randomized studies. These approaches may help define the patient populations and treatment settings in which quercetin could have therapeutic value in OSCC.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156710"},"PeriodicalIF":3.7,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149245511","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":"Advances in microfluidic chip technologies for the study and management of gastrointestinal cancers.","authors":"Noushin Nabavi, Milad Ashrafizadeh","doi":"10.1016/j.prp.2026.156706","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156706","url":null,"abstract":"<p><p>Gastrointestinal cancers (GICs) remain a major global health burden due to late-stage diagnosis, limited therapeutic efficacy, and poor prognosis. Conventional diagnostic and treatment strategies are often invasive, costly, and lack real-time monitoring capabilities, highlighting the need for the innovative and patient-centered approaches. This review critically examines the recent advances in microfluidic chip technologies for the diagnosis, modeling, and treatment of GICs, including gastric, colorectal, liver, pancreatic, and esophageal cancers. Microfluidic platforms enable the precise manipulation of microscale fluids, offering advantages such as reduced reagent consumption, high sensitivity, and integration of multiplexed assays into portable systems. Notably, recent studies demonstrate diagnostic performance with area under the curve (AUC) values exceeding 0.90 and sensitivities approaching 90%, while detection limits for key biomarkers such as ctDNA and proteins have reached attomolar (10⁻¹⁸ M) and picogram-per-milliliter levels. Applications discussed include circulating tumor cell (CTC) isolation, exosome and ctDNA detection, tumor-on-chip models, and microfluidic drug delivery systems. In addition, advances in materials, fabrication techniques, and fluid dynamics are evaluated for their role in optimizing device performance. Emerging integrations with machine learning further enhance diagnostic accuracy and predictive capability. Despite these promising developments, challenges related to standardization, scalability, and clinical validation remain. Overall, microfluidic technologies represent a transformative platform for enabling rapid, minimally invasive, and highly sensitive approaches to cancer diagnosis and personalized therapy in gastrointestinal oncology.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156706"},"PeriodicalIF":3.7,"publicationDate":"2026-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149244752","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":"Corrigendum to \"Anti-cancer effect of microRNA-139-3p on laryngeal squamous cell carcinoma by targeting rab5a: In vitro and in vivo studies\" [Pathol.-Res. Pract., 216(2020)153194].","authors":"Yifei Ma, Zhengpeng Gong, Huigang Wang, Ya Liang, Xin Huang, Guodong Yu","doi":"10.1016/j.prp.2026.156708","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156708","url":null,"abstract":"","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":" ","pages":"156708"},"PeriodicalIF":3.7,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149148807","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":"CircRNA hsa_circ_0001946 promotes hypertrophic scar pathogenesis via the miR-514a-3p/COL5A2 axis.","authors":"Yi Shi, Yajuan Song, Tong Wang, Yan Jiao, Yufei Zhang, Shu'ao Xiao, Baoqiang Song, Zhou Yu","doi":"10.1016/j.prp.2026.156641","DOIUrl":"10.1016/j.prp.2026.156641","url":null,"abstract":"<p><p>Hypertrophic scars (HSs) represent a fibroproliferative disorder characterized by excessive extracellular matrix deposition. However, the underlying regulatory mechanisms involving circular RNAs (circRNAs) have not yet been fully elucidated. This study aimed to delineate the circRNA expression landscape in HS and reveal the functional roles of a specific candidate circRNA through the competing endogenous RNA (ceRNA) network. Eighty-one differentially expressed circRNAs (DEcircRNAs) were identified in five paired HS and normal skin samples by high-throughput sequencing. Functional enrichment analysis of host genes highlighted pathways involving cell proliferation and ECM-receptor interactions. CircRNA-miRNA-mRNA network analysis revealed hsa_circ_0001946 as a significantly upregulated candidate circRNA. Subsequent RT-qPCR validated its elevation in human HS tissues and hypertrophic scar fibroblasts (HSFs). Subcellular fractionation and RNase R assays confirmed its cytoplasmic localization and circular stability. Functionally, knockdown of hsa_circ_0001946 significantly inhibited HSF proliferation, migration, and collagen gel contraction. Mechanistically, dual-luciferase reporter assays demonstrated that hsa_circ_0001946 acts as a sponge for miR-514a-3p; notably, silencing hsa_circ_0001946 attenuated the pro-fibrotic effects induced by miR-514a-3p inhibition. Furthermore, miR-514a-3p was shown to directly target and suppress COL5A2. Collectively, these findings establish that hsa_circ_0001946 promotes HS development by sequestering miR-514a-3p to derepress COL5A2 expression. This study identifies the hsa_circ_0001946/miR-514a-3p/COL5A2 axis as a novel pathogenic mechanism contributing to HS formation, suggesting hsa_circ_0001946 as a promising intervention target for mitigating pathological scarring.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"286 ","pages":"156641"},"PeriodicalIF":3.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685371","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":"Dysregulated autophagy in osteoarthritis: Mechanisms, regulation by non-coding RNAs, and therapeutic implications.","authors":"Liang Liu, Jie Wang, Lu Liu, Wenling Shi, Huajie Gao, Lun Liu","doi":"10.1016/j.prp.2026.156695","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156695","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a degenerative disease driven by inflammation, cell death, and metabolic changes. Autophagy is known as a cellular recycling process that plays a critical dual role in OA. It protects cartilage by removing damaged parts; however, excessive autophagy induces damages to chondrocytes. The way autophagy is dysregulated in OA was investigated and major areas, including the regulation of autophagy by non-coding RNAs (miRNAs, lncRNAs, circRNAs), the complex interaction of autophagy with cell death pathways such as apoptosis, pyroptosis, ferroptosis, and necroptosis were highlighted. In addition, the therapeutic potential of natural compounds and drugs that target autophagy were assessed. Notably, the protective versus detrimental effects of autophagy, which depends on disease stage and stress intensity, were discussed. Practical limitations, including the poor bioavailability of phytochemicals and the need for nano-delivery systems were highlighted. The paper concludes with proposing future research directions such as exploring autophagy-ferroptosis crosstalk.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"288 ","pages":"156695"},"PeriodicalIF":3.7,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149224807","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":"B4GALNT4 promotes lung cancer progression by suppressing ferroptosis through glycosylation of SLC7A11","authors":"Song Wu ,&nbsp;Rongrong Shen ,&nbsp;Shaofei Cheng ,&nbsp;Zhengyang Fan ,&nbsp;Hongyang Sang ,&nbsp;Qianping Li","doi":"10.1016/j.prp.2026.156548","DOIUrl":"10.1016/j.prp.2026.156548","url":null,"abstract":"<div><div>β-1,4-N-acetylgalactosaminyltransferase 4 (B4GALNT4) catalyzes LacdiNAc glycan synthesis and is implicated in multiple cancers; however, its role in lung cancer remains unclear. This study aimed to investigate the clinical relevance, biological impact, and regulatory pathways of B4GALNT4 in lung cancer. B4GALNT4 expression across 33 cancers was analyzed using Gene Expression Profiling Interactive Analysis, and its level, prognostic relevance, and pathways enrichment in lung cancer were further assessed. Its effects on cell viability, cell cycle, and ferroptosis were evaluated with gain- and loss-of-function assays. Co-immunoprecipitation, protein stability assays, immunofluorescence, and Western and lectin blotting were performed to identify whether B4GALNT4 regulates solute carrier family 7 member 11 (SLC7A11) glycosylation. Rescue experiments were conducted to verify whether B4GALNT4 affected the malignant proliferation phenotype via the SLC7A11-mediated ferroptosis pathway. B4GALNT4 is upregulated, and its upregulation is associated with a worse prognosis in lung cancer. Gene Set Enrichment Analysis demonstrated enrichment of proliferation and cell cycle pathways, alongside ferroptosis suppression in B4GALNT4 high-expression samples. Functional experiments revealed that B4GALNT4 knockdown significantly inhibited lung cancer cell viability by 25.6% and induced a 1.92-, 2.03-, 1.76-, and 4.29-fold increase in the cell proportion in G1 phase, intracellular Fe²⁺, malondialdehyde levels, and lipid reactive oxygen species production (<em>P</em> &lt; 0.001), respectively, which were reversed by Fer-1 <em>in vitro</em> (<em>P</em> &lt; 0.001) and <em>in vivo</em> (<em>P</em> &lt; 0.05). Conversely, B4GALNT4 overexpression improved the resistance of cells to ferroptosis (<em>P</em> &lt; 0.001). Mechanistically, we discovered that B4GALNT4 interacted with SLC7A11 and glycosylated it at residue N314. This N-glycosylation stabilized SLC7A11 and promoted membrane localization by blocking its degradation, which promoted cell viability and cell cycle progression and inhibited ferroptosis. Our findings establish B4GALNT4 as a critical regulator of lung cancer through SLC7A11 glycosylation, indicating that B4GALNT4 and SLC7A11 serve as potential therapeutic targets for lung cancer.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"285 ","pages":"Article 156548"},"PeriodicalIF":3.2,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148000389","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":"YAP-induced BICD1 promotes hepatocellular carcinoma cell proliferation, stemness, and migration by facilitating the nuclear translocation of HIF-1α.","authors":"Yezhen Jiang, Siying Jia, Chengquan Zhang, Lei Zhang, Kangsheng Tu, Qingguang Liu","doi":"10.1016/j.prp.2026.156540","DOIUrl":"https://doi.org/10.1016/j.prp.2026.156540","url":null,"abstract":"<p><p>Treatment options for hepatocellular carcinoma (HCC) remain limited, and patient prognosis is generally poor. Therefore, elucidating the molecular mechanisms underlying HCC initiation and progression is critical for identifying novel therapeutic targets. Our previous study demonstrated that BICD cargo adaptor 1 (BICD1) was upregulated in HCC and functioned as a tumor promoter. However, the upstream regulators of BICD1 expression and the molecular basis of its pro-tumorigenic effects remain unclear. In this study, we identified Yes-associated protein (YAP) as a positive regulator of BICD1 in HCC. Mechanistically, YAP directly bound to the BICD1 promoter and enhanced its transcriptional activity. BICD1 expression was positively correlated with YAP, connective tissue growth factor (CTGF), and cysteine-rich angiogenic inducer 61 (CYR61) in HCC tissues. Functionally, BICD1 knockdown significantly attenuated hypoxia-induced proliferation, sphere formation, and migration of HCC cells, whereas BICD1 overexpression enhanced these phenotypes. In addition, BICD1 depletion markedly suppressed tumor initiation and growth in a nude mouse model. Further mechanistic investigations revealed that BICD1 interacted with hypoxia-inducible factor-1α (HIF-1α) via its C-terminal CC3 domain, thereby promoting HIF-1α nuclear translocation and transcriptional activity in HCC cells. Notably, AKT activation or knockdown of glycogen synthase kinase 3β (GSK3β) significantly enhanced the interaction between BICD1 and HIF-1α, thereby increasing HIF-1α transcriptional activity. Collectively, these findings demonstrate that YAP-driven BICD1 expression facilitates HIF-1α nuclear translocation and activation of downstream target genes, thereby promoting hypoxia-induced proliferation, stemness, and migration in HCC. This study highlights the YAP-BICD1-HIF-1α axis as a potential therapeutic target in HCC.</p>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":" ","pages":"156540"},"PeriodicalIF":3.2,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147974585","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":"Granulocytic myeloid derived suppressor cells derived extracellular vesicles ameliorate DSS-induced colitis via modulation of Th17/Treg balance","authors":"Juan Liu ,&nbsp;Chinenye Jane Ugwah-Oguejiofor ,&nbsp;Ling Zhu","doi":"10.1016/j.prp.2026.156405","DOIUrl":"10.1016/j.prp.2026.156405","url":null,"abstract":"<div><div>Colitis is closely associated with immune system dysregulation in the gastrointestinal tract. The present study aimed to evaluate the impact of Granulocytic Myeloid-Derived Suppressor Cells (G-MDSCs)-derived extracellular vesicles (EVs) on disease activity and the immunologic profile in a murine model of colitis. G-MDSCs-EVs were administered to colitis-bearing mice and were evaluated for changes in body weight, disease activity index, colon histopathology, frequencies of Th17 and Tregs, and cytokine release from lymphocytes. The impact of G-MDSCs-EVs was also evaluated on the expression of immune-response-related genes and the intestinal microbiome. G-MDSCs-EVs prevented body weight loss and controlled the disease activity index on day 10. This treatment improved the Treg population along with a decrease in the release of IL-6, IL-17A, and IFN-γ from lymphocytes. Treatment with G-MDSCs-EVs modulated immune-response-related gene expression and influenced the gut microbiota and colon histopathology. G-MDSCs-EVs demonstrated a preliminary potential in expanding the Treg population and upregulating immunoregulatory cytokines, which contributed to improvements in disease activity index and histopathology of the affected tissue.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"281 ","pages":"Article 156405"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146196842","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}