Experimental Biology and Medicine最新文献

{"title":"The value of serum exosomal miRNA signature profiles for the early diagnosis of feline infectious peritonitis.","authors":"Hongxia Gu, Huisheng Wu","doi":"10.3389/ebm.2026.10915","DOIUrl":"10.3389/ebm.2026.10915","url":null,"abstract":"<p><p>Feline Infectious Peritonitis (FIP) is a highly lethal disease in cats, and early differential diagnosis remains a significant clinical challenge. In this study, we analyzed differences in serum exosomal miRNA expression between FIP-affected cats and healthy control cats via high-throughput sequencing and identified five significantly differentially expressed miRNAs (miR-21-5p, miR-155-5p, miR-200c-3p, miR-486-5p, and miR-423-5p). A combined diagnostic model was constructed based on three key miRNAs (miR-21-5p, miR-155-5p, and miR-423-5p). ROC curve analysis showed that a combined model of these three key miRNAs had an area under the curve (AUC) of 0.93, with a sensitivity and specificity of 88.6% and 91.2%, respectively. These results indicate that the serum exosomal miRNA signature could be used as a novel biomarker for the early diagnosis of FIP, providing a non-invasive diagnostic tool in clinical practice.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10915"},"PeriodicalIF":3.8,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13503298/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817979","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":"XPA confers ability of endonucleases to act processively and to incise damaged nucleosomal DNA.","authors":"Muriel W Lambert, W Clark Lambert","doi":"10.3389/ebm.2026.10902","DOIUrl":"10.3389/ebm.2026.10902","url":null,"abstract":"<p><p>Repair of damaged DNA is a complex process, particularly when it is compacted into nucleosomes. There are a number of genetic disorders with deficiencies in DNA repair. Knowledge of the genes and proteins involved in these repair deficiencies is critical in developing an understanding of the molecular mechanisms utilized by proteins in the DNA repair pathways. One of these genetic disorders is xeroderma pigmentosum (XP), which is defective in nucleotide excision repair (NER). Patients in XP complementation group A (XP-A) are among the most severely affected with the lowest levels of DNA repair. The XPA protein, which is defective in these patients, plays a number of roles in the DNA repair process. One particularly important role proposed is acting as a processivity factor enabling endonucleases (XPF and XPG) and the XPB/TFIIH translocase to localize to damage sites using a processive mechanism of action. Another proposed role is in interacting with chromatin-remodeling proteins so as to enhance accessibility of lesions in nucleosomal DNA to endonucleolytic incision and other DNA repair activities. In XP-A cells, the XPA protein is proposed to be defective in ability to act as a processivity factor; endonucleases localize damage sites by a distributive mechanism and are also defective in incision of damaged nucleosomal DNA. This defect is corrected by recombinant normal human XPA. Mutations in exons 3 and 5 in the DNA binding domain of the <i>XPA</i> gene lead to loss of ability of XPA to act as a processivity factor. The mutation in exon 5 was found in two XP-A patients with severe XP. These studies emphasize the importance of correlating specific mutations in an XP gene and the resulting defect in a particular repair protein with the clinical severity of XP and could lead to development of novel therapeutic approaches for this disorder.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10902"},"PeriodicalIF":3.8,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13505299/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148817959","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":"The role and mechanism of neutrophils in oncolytic virus therapy.","authors":"Baixian Huang, Qixin Yang, Ruixue Wang, Chaochao Zhao","doi":"10.3389/ebm.2026.11192","DOIUrl":"https://doi.org/10.3389/ebm.2026.11192","url":null,"abstract":"<p><p>Oncolytic viruses (OVs) are a class of viruses capable of specifically infecting and killing tumor cells. They exert antitumor effects through direct lysis of tumor cells, activation of the immune system, and disruption of tumor vasculature. Neutrophils, which originate from the bone marrow, are the most abundant leukocytes in peripheral blood and the immune system and play a dual regulatory role in oncolytic virotherapy. In different TME, neutrophils can polarize into two phenotypes: N1 and N2. N1 neutrophils, owing to their chemotaxis and tumor-homing capabilities, can serve as delivery vehicles for OVs, enhance the therapeutic efficacy of oncolytic virotherapy, and activate host immune responses. In contrast, N2 neutrophils impair the efficacy of OVs through their antiviral activity and immunosuppressive functions. Therefore, an in-depth understanding of the mechanisms underlying the role of neutrophils in oncolytic virotherapy is of great significance for optimizing OV-based therapies and improving their clinical application outcomes.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11192"},"PeriodicalIF":3.8,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13489981/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790032","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":"Correction: Protective effects of berberine-loaded chitosan/solid lipid nanoparticles in streptozotocin-induced gestational diabetes mellitus rats.","authors":"","doi":"10.3389/ebm.2026.10958","DOIUrl":"https://doi.org/10.3389/ebm.2026.10958","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/ebm.2025.10749.].</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10958"},"PeriodicalIF":3.8,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148790028","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":"Causal association between clonal hematopoiesis indeterminate potential and cancer: a Mendelian randomization study.","authors":"Juan Jin, Qian Pu, Chengrong Wu, Yu Lei, Yaxin Hu, Xiuju Yang, Jinghui Huang, Fangfang Wu, Li Xiao, Lei Yu","doi":"10.3389/ebm.2026.10923","DOIUrl":"10.3389/ebm.2026.10923","url":null,"abstract":"<p><p>Clonal hematopoiesis of indeterminate potential (CHIP) causes the expansion of mutated hematopoietic stem cells and produces immunophenotypically altered leukocytes, which induce a tumor-promoting inflammatory condition. However, the causal effect of CHIP on cancer remains unclear. We assessed the relationship of genetically predicted CHIP with the risk of 18 cancer types involving 612,576 cases using two-sample Mendelian randomization (MR). Genetic instruments for overall and sub-types of CHIP were obtained from the a large-scale genome-wide association study using independent (r² < 0.001) SNPs at genome-wide significance (p < 5.0 × 10^-8). Summary statistics for 18 cancers were obtained from the FinnGen, MVP, PLCO study, and large consortia. Inverse-variance weighted random-effects models were used as the primary method for estimating causal effects. Findings from independent datasets were combined using the fixed-effect model and Bonferroni corrections were applied for multiple testing. We found genetic predicted overall and DNMT3A CHIP was significantly associated with an increased risk of thyroid cancer, lung cancer, kidney cancer, brain cancer, basal cell carcinoma, and malignant melanoma after corrections. In addition, we found the causal estimate of CHIP varied across histological sub-types of cancer. Sensitivity analyses confirmed that these findings were robust. Strong associations were found between genetic predicted CHIP and an increased risk of a broad range of cancers, highlighting the importance of timely screening for CHIP in cancer early detection and prevention.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10923"},"PeriodicalIF":3.8,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13455644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705902","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":"Novel perspective on immune cell regulation in gastrointestinal inflammation: the role of extracellular vesicles and therapeutic prospects.","authors":"Jianshu Wang, Junxuan Xu, Zilu Cui, Jing Wu","doi":"10.3389/ebm.2026.11114","DOIUrl":"10.3389/ebm.2026.11114","url":null,"abstract":"<p><p>Gastrointestinal inflammation is an inflammatory disease arising from immune imbalance in any segment of the digestive tract, triggered by various factors. Immune cells play important roles in both the onset and resolution of gastrointestinal inflammation. With the recent extensive research on extracellular vesicles, the mechanism by which immune cells regulate gastrointestinal inflammation through extracellular vesicles has gradually gained recognition within the scientific community. Extracellular vesicles derived from immune cells can communicate with other immune cells in the digestive tract and directly regulate digestive tract epithelial cells. Furthermore, with advances in biological nanotechnology, immune cell-derived extracellular vesicles may be used to treat inflammatory gastrointestinal diseases. This review focuses on delineating the role of immune cell-derived extracellular vesicles in gastrointestinal inflammation and exploring their potential applications in treating these inflammatory diseases.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11114"},"PeriodicalIF":3.8,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13423738/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652965","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":"Genetic evidence for causal relationships between brain functional networks and domain-specific recovery after nondisabling ischemic stroke.","authors":"Huan Cai, Zhenchun Huang, Jialin Liang, Hao Zhang, Zhonghua Liu","doi":"10.3389/ebm.2026.10948","DOIUrl":"10.3389/ebm.2026.10948","url":null,"abstract":"<p><p>Intrinsic brain networks are crucial for post-stroke recovery, but the causal relationships between specific networks and domain-specific recovery outcomes, as well as the role of lipid metabolism, remain unclear. This study leveraged Mendelian randomization (MR) to evaluate 191 resting-state functional magnetic resonance imaging (rs-fMRI) BOLD-derived phenotypes in relation to post-stroke recovery after nondisabling ischemic stroke. Genetic instruments for rs-fMRI phenotypes were derived from a UK Biobank genome-wide association study (n = 34,691). Outcomes included motor, cognitive, and global recovery after nondisabling ischemic stroke, assessed using longitudinal National Institutes of Health Stroke Scale subscales over 2 years (n = 1,270). Primary analyses used the multiplicative random-effects inverse-variance weighted method. A two-step MR analysis investigated whether brain networks mediate the effects of lipids on post-stroke outcomes. Higher BOLD-derived functional connectivity within the triple network (default mode network, central executive network, and salience network) was associated with better motor and cognitive outcomes. Higher genetically predicted orbitofrontal node amplitude in the limbic network correlated with better motor recovery, while stronger parieto-frontal connectivity was associated with cognitive recovery. Genetically proxied higher low-density lipoprotein cholesterol (LDL-C) was associated with poorer cognitive recovery, with evidence suggesting partial mediation through differences in BOLD-derived triple-network connectivity. This MR study supports a potential causal role of BOLD-derived functional network phenotypes, particularly the triple network, in motor and cognitive recovery, and further suggests that differences in triple-network connectivity act as a partial mediator linking elevated LDL-C liability to impaired cognitive recovery. These findings provide hypothesis-generating evidence for future mechanistic studies and for exploring whether specific brain network-targeted interventions could have a role in stroke recovery.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10948"},"PeriodicalIF":3.8,"publicationDate":"2026-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13402224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600864","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":"Gut microbiota and polyendocrine metabolic ovarian syndrome: an integrated gut-metabolism-endocrine-ovary axis.","authors":"Shengyue Jin, Menglei Zhu, Yiyang Lu, Jia Zhao, Jiayi Zhu, Xiaohong Fang","doi":"10.3389/ebm.2026.11058","DOIUrl":"10.3389/ebm.2026.11058","url":null,"abstract":"<p><p>Polyendocrine metabolic ovarian syndrome (PMOS), previously known as polycystic ovary syndrome (PCOS), is a common endocrine and metabolic disorder in reproductive-age women, characterized by marked clinical and biological heterogeneity. Accumulating evidence suggests that gut microbiota dysbiosis is associated with metabolic disturbances, hormonal imbalance, and ovarian dysfunction in PMOS. However, the pathways linking gut microbiota alterations to PMOS pathogenesis remain incompletely understood, and most evidence remains associative. This review aims to summarize current evidence regarding interactions between gut microbiota and PMOS, clarify the roles of key microbiota-derived metabolites, and evaluate the potential and limitations of gut microbiota-targeted interventions. A major novelty is the proposal of an integrated gut-metabolism-endocrine-ovary axis incorporating phenotypic heterogeneity, methodological variability, and evidence grading across clinical and preclinical studies. A narrative review with a systematic literature search was conducted. PubMed, Web of Science, Embase, and CNKI were searched from inception to March 2026 using terms related to PMOS, gut microbiota, microbial metabolites, and microbiota-targeted interventions. Eligible studies included human observational or interventional studies, animal experiments exploring microbiota-PMOS mechanisms, and peer-reviewed full-text articles in English or Chinese. Case reports, letters, conference abstracts, non-English publications, and irrelevant studies were excluded. Duplicate records were removed. Two authors independently screened records and resolved disagreements by consensus. No meta-analysis was performed, and clinical registration was not applicable. Gut microbiota dysbiosis may contribute to PMOS through chronic low-grade inflammation, insulin resistance, and hyperandrogenism. Microbiota-derived metabolites link intestinal dysbiosis with metabolic and endocrine dysfunction. Bile acids and short-chain fatty acids exert regulatory effects, whereas amino acid disorders and LPS-mediated endotoxemia amplify metabolic and inflammatory abnormalities. Considerable heterogeneity exists across studies regarding obesity, insulin resistance, hyperandrogenism, diet, ethnicity, region, and methodology. Microbiota-targeted interventions show potential, although evidence quality varies and most findings remain associative. Gut microbiota dysbiosis is a critical regulatory node within the integrated gut-metabolism-endocrine-ovary axis in PMOS. This review highlights phenotypic stratification, evidence hierarchy, and clinical translation potential. Although microbiota-targeted strategies may serve as adjunctive therapies, their causal roles and long-term efficacy require confirmation in well-designed longitudinal and randomized controlled trials.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11058"},"PeriodicalIF":3.8,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13395754/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148583933","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":"A whole-transcriptome analysis of differentially expressed genes, transcripts, and transcript usage in blood samples from Parkinson's disease patients.","authors":"Sulev Koks, Mari Muldmaa, Jack Price, Luke Whiley, Maili Jakobson, Lewis Singleton, Denise Howting, Abigail L Pfaff, Abha Chopra, Mark Watson, Katrin Sikk, Pille Taba","doi":"10.3389/ebm.2026.11099","DOIUrl":"10.3389/ebm.2026.11099","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a complex neurodegenerative disorder with diverse molecular signatures that extend beyond the central nervous system. Peripheral blood serves as a minimally invasive source of transcriptomic biomarkers reflecting systemic inflammation, mitochondrial dysfunction, lysosomal impairment, and disrupted RNA processing-key pathways involved in PD. Long-read RNA sequencing with Oxford Nanopore Technologies (ONT) offers unprecedented detail of full-length transcripts, alternative isoforms, and RNA modifications, enabling more accurate detection of disease-related transcriptional changes. We conducted high-throughput ONT long-read RNA sequencing on blood samples from 145 individuals, including PD patients and age-matched healthy controls. RNA libraries were prepared using a cDNA-based protocol optimised for high-accuracy PromethION sequencing. Transcriptomes were quantified with ONT-specific pipelines, and analyses of differential gene expression (DGE), differential transcript expression (DEX), differential transcript usage (DTU), and alternative splicing were performed using ONT-aware tools such as DRIMSeq, DEXSeq, and stageR. Pathway enrichment linked disease-related changes to mitochondrial, lysosomal, and vesicle-trafficking pathways. Our analysis identified highly significant PD-associated transcriptional signatures in peripheral blood (SNCA, VPS13C, LRRK2, GRN, STAU1, NPTN, PARK7). Long-read sequencing uncovered extensive isoform-level dysregulation, including novel transcript variants (e.g., BCL2L2-PABPN1, SQSTM1) in pathways relevant to PD, such as autophagy and endolysosomal trafficking. DTU analyses revealed shifts in isoforms of LRRK2 and GBA1, indicating widespread disturbances in RNA processing. Enrichment analysis showed activation of molecular pathways linked to neurodegeneration. This study provides the largest long-read blood transcriptomic dataset in PD to date, demonstrating that ONT sequencing can resolve isoform-level changes and reveal systemic molecular signatures of PD. Our findings support the development of blood-based RNA biomarkers and the establishment of long-read transcriptomics as a transformative approach for genomic pathology in PD.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11099"},"PeriodicalIF":3.8,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13388229/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148561300","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":"Transcriptomics-based identification of shared biomarkers across type 2 diabetes, mild cognitive impairment, and uric acid metabolism.","authors":"Yan Liu, Dongmei Kang, Yuan Lei","doi":"10.3389/ebm.2026.11060","DOIUrl":"10.3389/ebm.2026.11060","url":null,"abstract":"<p><p>Uric acid metabolism is associated with the development of type 2 diabetes mellitus (T2DM), cardiometabolic, and cardiovascular diseases. Additionally, T2DM patients often exhibit mild cognitive impairment (MCI). However, the underlying mechanisms remain unclear. This study aims to identify and validate biomarkers associated with uric acid metabolism in T2DM and MCI, with the goal of discovering potential diagnostic and therapeutic targets to improve the quality of life for T2DM patients. Transcriptomic data for T2DM, MCI and uric acid metabolism-related genes were sourced from public databases. Biomarkers were screened using machine learning and validated for expression. Subsequent analyses included functional enrichment, immune infiltration, subcellular localization, and drug prediction. Three biomarkers-HP, ITGB3, and SELP-were identified. All showed significantly elevated expression in the T2DM group (p < 0.05). HP and ITGB3 were primarily enriched in ribosome-related pathways, primary immunodeficiency, and adherens junction processes. Immune infiltration analysis revealed that immature B cells and plasmacytoid dendritic cells were significantly enriched in T2DM. HP showed the strongest positive correlation with plasmacytoid dendritic cells (cor = 0.65, FDR <0.05), while ITGB3 exhibited the strongest positive correlation with immature B cells (cor = 0.76, FDR <0.05). Several potential therapeutic drugs were predicted, including calcifediol (score = -99.93) and meclofenamic acid (score = -99.89). This study identified three candidate biomarkers co-dysregulated across T2DM and MCI transcriptomes and associated with uric acid metabolism. Given the exploratory sample sizes, these findings are considered hypothesis-generating and require validation in larger independent cohorts.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11060"},"PeriodicalIF":3.8,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13381339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600856","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}