Experimental Biology and Medicine最新文献

{"title":"Training the next-generation of biomedical scientists through artificial intelligence-driven education and research in pharmacology and pharmaceutical sciences.","authors":"Santosh Kumar, Ritu Karwasra, Weinan Zhou, Jayaraman Seetharaman, Bhupesh Singla","doi":"10.3389/ebm.2026.10988","DOIUrl":"https://doi.org/10.3389/ebm.2026.10988","url":null,"abstract":"<p><p>Artificial intelligence (AI)-driven graduate education and research in pharmacology and pharmaceutical sciences (AIPPS) aims to address the rapidly-growing role of AI and machine learning (ML) applications in biomedical sciences. This review provides perspectives on why and how the next-generation of biomedical scientists equip themselves with skills necessary to integrate AI and ML tools into their current fields of study, particularly pharmacology and pharmaceutical sciences. The AI-enabled approaches discussed in this article highlight opportunities for improving competitiveness in an evolving scientific landscape, that includes academia, pharmaceutical and biotech industries and regulatory science. Furthermore, this review discusses how graduate education and research can be enhanced through training in AI-driven disease prediction, molecular target identification drug design and discovery, drug repurposing and pharmacometric modelling. The knowledge outlined here may help graduate students and early career researchers navigate the challenges associated with applying AI-based methodologies in fundamental research, product and process development, service delivery, and regulatory policy and ethics. Overall, the insights provided in the review aim to support the development of skilled forward-thinking biomedical and pharmaceutical scientists capable of leveraging AI technologies in modern research environments.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10988"},"PeriodicalIF":2.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143847/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147835796","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":"Elevated ApoC3 levels in cerebrospinal fluid predict poor outcomes in patients with aneurysmal subarachnoid hemorrhage.","authors":"Bin Tong, Junjie Wang, Jiarui Chen, Qia Zhang, Zhouhan Xu, Kaichuang Yang, Xiaomin Chen","doi":"10.3389/ebm.2026.10827","DOIUrl":"https://doi.org/10.3389/ebm.2026.10827","url":null,"abstract":"<p><p>Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating condition associated with approximately 30% mortality and 20% severe disability among survivors. Delayed cerebral ischemia due to cerebral vasospasm and hydrocephalus significantly contribute to poor neurological outcomes. Currently, reliable biomarkers for early prediction of these complications remain lacking. In this study, 63 patients with a mean age of 59.7 ± 11.53 years were enrolled. Functional outcomes were assessed by the modified Rankin Scale (mRS). Cerebrospinal fluid (CSF) samples were obtained through lumbar drainage (LD) or external ventricular drainage (EVD) and analyzed by ELISA. The predictive value of biomarkers was evaluated using receiver operating characteristic (ROC) curve analysis. Elevated Apolipoprotein C-III (ApoC3) levels in CSF of aSAH patients were observed. Furthermore, increased ApoC3 concentrations were significantly associated with poor prognosis and an elevated risk of severe complications. At an optimal cutoff value of 4,463 ng/mL, patients with high ApoC3 levels exhibited significantly worse 3-month functional outcomes and a higher incidence of delayed cerebral ischemia and hydrocephalus. Monitoring ApoC3 levels in CSF may be beneficial for predicting complications such as delayed cerebral ischemia and hydrocephalus in patients with aSAH.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10827"},"PeriodicalIF":2.7,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13132793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812771","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":"CAR T cell engineering approaches to minimise toxicities.","authors":"Elizabeth Hogben, Anna Schurich, Charlotte Graham","doi":"10.3389/ebm.2026.11021","DOIUrl":"https://doi.org/10.3389/ebm.2026.11021","url":null,"abstract":"<p><p>For the treatment of many forms of cancer, cell- and gene-based therapies are showing promise in both pre-clinical data and clinical trials. In particular, CAR T cell therapies, of which there are now 7 FDA-approved products, have shown ground-breaking results in haematological cancers such as multiple myeloma and B cell malignancies. Recent research is also attempting to develop effective CAR T cell therapies for solid tumours, with varying success. One of the key challenges faced by CAR T cell therapy is balancing strong cytotoxic activity for an effective treatment with preventing severe and potentially lethal toxicities, such as Cytokine Release Syndrome and Immune Effector Cell-Associated Neurotoxicity Syndrome. This mini review discusses some of the potential solutions that scientists have devised to overcome toxicities and improve existing CAR T cell therapies.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11021"},"PeriodicalIF":2.7,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13124637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147812710","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":"Lymphatic pumping technique in mice alters blood parameters and metastatic melanoma in an age-dependent manner.","authors":"Christopher Walsh, Matthew Kirstein, Elise Wagner, Emily Scott, Jerome Walsh, Shashank Reddy, Nathan Hoggard, Arshad Ahmad, Reetobrata Basu, Sam Mathes, Yanrong Qian, John J Kopchick","doi":"10.3389/ebm.2026.10850","DOIUrl":"https://doi.org/10.3389/ebm.2026.10850","url":null,"abstract":"<p><p>Therapeutic touch applied to primary tumors can increase metastasis. The goal of this project was to determine whether touch applied to metastatic tumors also increases metastasis. We evaluated touch on a mouse model of experimental metastasis using a manual treatment called Lymphatic Pumping Technique (LPT), which increases lymphatic fluid flow and is contraindicated in patients with cancer. The LPT, or a sham treatment, was administered for 5 minutes while the mice were anesthetized with vaporized isoflurane. Young adult (3 months old) and aged (20-24 months old) mice received daily sham or LPT treatments for 7 days prior to the injection of 200k B16F10-luc2 mouse melanoma cells into the tail vein, then treated every other day for 21 days. In middle-aged (9-11 months old) mice, we waited 8 days after tumor injection to start treatments and assessed the effect of LPT on immunotherapy efficacy. These mice also received either LPT or sham every other day, along with four doses of 200 µg anti-PD-1 or isotype control antibody. LPT did not increase tumor growth or spread in any of the experiments. Surprisingly, LPT was negatively associated with metastasis in young and middle-aged mice, without enhancing or diminishing the efficacy of immunotherapy. In mice without cancer, LPT rapidly elevated red blood cell, white blood cell, and platelet counts in young, but not middle-aged, animals. Taken together, these findings suggest that therapeutic touch near metastatic tumors does not worsen disease and may confer an age-dependent benefit.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10850"},"PeriodicalIF":2.7,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13071501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147689057","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":"Towards a standardized diabetic prolonged wound healing model in hairless SKH1 mice.","authors":"Elle Koivunotko, Julia Monola, Chris S Pridgeon, Jere Linden, Riina Harjumäki, Emrah Yatkin, Mari Madetoja, Marjo Yliperttula","doi":"10.3389/ebm.2026.10857","DOIUrl":"https://doi.org/10.3389/ebm.2026.10857","url":null,"abstract":"<p><p>Chronic wounds, particularly those associated with diabetes, pose a significant clinical challenge due to their impaired healing dynamics and lack of reliable and standardized preclinical models. This pilot study aimed to establish a diabetogenic, immunocompetent, hairless mouse model (SKH1 strain) to simulate prolonged wound healing. Diabetes was induced by streptozotocin administration, followed by the creation of full-thickness dorsal skin wounds. Wounds were treated with either saline or nanofibrillated cellulose hydrogel as a model treatment. Wound healing progression and blood glucose were monitored, and histopathological assessments were performed after a 14-day experiment. In addition, for the first time, the Thermidas thermal imaging system was used in an <i>in vivo</i> mouse model to evaluate skin temperature. Results demonstrated that diabetes induction successfully prolonged wound closure by 5 days compared with the previously described acute wound model in the same strain with the identical protocol without streptozotocin (STZ) induction. Histopathological analyses showed increased macrophage activity (16.2% vs. 2.2% in the treatment groups and 10.2% vs. 0.3% in the control groups) and decreased collagen deposition (12.2% vs. 43.2% in the treatment groups and 17.6% vs. 27.4% in the control groups), suggesting prolonged wound healing. These findings support the use of hairless SKH1 mice as a viable model for studying prolonged diabetic wound healing and evaluating future therapeutic candidates.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10857"},"PeriodicalIF":2.7,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13046712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622075","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":"Genetics of epilepsy.","authors":"Kynen Piacentini, Athanasios Gaitatzis, Sulev Kõks","doi":"10.3389/ebm.2026.10933","DOIUrl":"https://doi.org/10.3389/ebm.2026.10933","url":null,"abstract":"<p><p>Epilepsy is one of the most common neurological diseases in the world, but it is also complex and difficult to study. There is a significant genetic component to epilepsy and more information is being published frequently. It is difficult to group and summarise all of this information in a way that is beneficial for both researchers and clinicians. The aim of this paper is to create a summary of all currently known epilepsy associated genes in order to aid epilepsy research to better understand the aetiology of the disease. This was achieved through gathering genetic data from three databases: Online Mendelian Inheritance in Man (OMIM), Clincal Genome (ClinGen), and PubMed. Genes were filtered based on specific criteria and were summarised into three tables: Epilepsy genes, Epilepsy associated genes and Predicted epilepsy associated genes. A fourth table was produced to showcase all epilepsy genes that were identified in all three databases. A total of 2,536 genes were identified to have some level of association with epilepsy. A total of 238 genes were classified as Epilepsy genes, 1,317 genes were classified as Epilepsy associated genes and 981 genes were classified as Predicted epilepsy genes. Finally, 86 genes were identified to be epilepsy genes that were found in all three genetic databases and represent the highest confidence in association with epilepsy. The significance of this study involves the ability to give researchers an up-to-date list of genes that have an association to epilepsy and a summary of information about said genes.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10933"},"PeriodicalIF":2.7,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13075117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147689046","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 novel platelet-rich plasma clinically induces reliable, rapid, long-term chronic peripheral neuropathic pain elimination.","authors":"Damien P Kuffler, Onix Reyes, Ivan J Sosa, Christian A Foy","doi":"10.3389/ebm.2026.10907","DOIUrl":"10.3389/ebm.2026.10907","url":null,"abstract":"<p><p>Peripheral nerve trauma results in 50%-84% of patients developing chronic neuropathic pain, which is eliminated when axons reinnervate targets. Autografts reduce pain by promoting target reinnervation. We hypothesized that applying a novel platelet-rich plasma (PRP) formulation to proximal stumps would permanently eliminate the pain. This prospective case series compared analgesia levels after bridging nerve gaps with an autograft (autograft repair) vs. a PRP-filled collagen tube (PRP repair). Autograft repairs were performed on 16 nerves with a 5.75-cm mean gap length, 2.0-year repair delay, 42.3-year age, and 8.6 chronic neuropathic pain. PRP repairs were performed on 10 nerves with a 6.0-cm gap length, 1-year repair delay, 36.7-year age, with 88% having 9.1 chronic neuropathic pain. For autograft repairs, the pain began to decrease when axons reinnervated targets, reaching a mean of 0.3 in 18.2% of patients, and was eliminated in 81.8%. Following PRP repairs, the pain reduction began within 2 weeks and was eliminated by 2 months. Thus, autografts contribute to pain reduction/elimination by promoting target reinnervation. However, PRP directly and rapidly induced long-term pain elimination in all patients, while axons were regenerating, and without target reinnervation. These results prove that platelet-released factors reliably and rapidly eliminate chronic neuropathic pain.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10907"},"PeriodicalIF":2.7,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573119","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":"Enhanced oxidative stress resilience in <i>C. elegans acox-1.1</i> mutants through CTL-3 and proteasomal regulation.","authors":"Woori Bae, Mina Norman, Myon Hee Lee","doi":"10.3389/ebm.2026.10796","DOIUrl":"10.3389/ebm.2026.10796","url":null,"abstract":"<p><p>Oxidative stress is a primary driver of aging, necessitating robust cellular adaptation mechanisms. While peroxisomal β-oxidation and proteasomal degradation are known to influence stress responses, their functional crosstalk remains elusive. In this study, we show that <i>C. elegans acox-1.1</i> mutants, despite having a shortened lifespan under normal conditions, exhibit a paradoxical resistance to mild chronic oxidative stress (1 mM paraquat, PQ) compared to wild-type worms. This PQ-induced resistance in <i>acox-1.1</i> mutants was independent of the canonical SKN-1 pathway but required the peroxisomal catalase CTL-3. RNA-mediated knockdown of <i>ctl-3</i> largely abolished the stress resistance of <i>acox-1.1</i> mutants, leading to rapid mortality. Proteomic and biochemical analyses revealed that <i>acox-1.1</i> mutants possess reduced levels of PAS-5, a core 20S proteasome subunit, resulting in impaired proteasomal assembly and accumulation of ubiquitinated (Ub) substrates under basal conditions. Intriguingly, exposure to 1 mM PQ significantly reduced the Ub-smear in <i>acox-1.1</i> mutants, suggesting a metabolic shift where the cell prioritizes ROS scavenging over ATP-dependent protein degradation. Under oxidative stress, <i>acox-1.1</i> mutants bypass defective proteasomal machinery and redirect energy toward CTL-3-mediated antioxidant defense. This study identified a peroxisomal adaptation mechanism whereby reduced proteasome complexity, coupled with enhanced ROS-regulatory machinery, confers survival advantages under specific oxidative challenges.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10796"},"PeriodicalIF":2.7,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573109","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":"Low dose thirdhand smoke exposure enhances platelet functional responses in mice.","authors":"Precious O Badejo, Ahmed B Alarabi, Hamdy E A Ali, Lanam Millican, Reina De La Paz, Shelby S Umphres, Sadia Kamal, Fatima Z Alshbool, Fadi T Khasawneh","doi":"10.3389/ebm.2026.10679","DOIUrl":"10.3389/ebm.2026.10679","url":null,"abstract":"<p><p>Although cigarette smoking is the most preventable cause of cardiovascular diseases, most researchers have focused on either direct/firsthand or secondhand smoke exposures. Recently though, attention has shifted to an emerging/indirect exposure trend-known as thirdhand smoke (THS)- which was previously \"overlooked.\" This phenomenon, which was/is thought to be harmless, has been identified as a serious health risk, including in the context of thrombogenesis/platelets. However, whether low dose THS exposure has the capacity to modulate platelets has not been investigated. Two sets of household materials were exposed to 20 cigarettes/day for a week on an alternating basis, with controls exposed to clean air. After the first set of exposed materials is placed in mice cages, exposure of the second set is initiated. The materials were interchanged weekly, for a total exposure duration of 1 month. Mice were then subjected to multiple platelet function assays. THS exposed mice exhibited shortened tail bleeding and occlusion times, indicating a prothrombotic phenotype. Moreover, we also observed that platelets from the exposed mice exhibited an enhanced aggregation response. However, we did not observe any gender differences in our <i>in vivo</i> as well as aggregation experiments; hence, subsequent characterization was carried out on male mice. It was also found that dense granules release, integrin activation, and PS exposure were also potentiated in the exposed platelets compared to the controls. Finally, we observed for the first time that the tobacco-specific nitrosamine and THS toxicant NNK enhanced platelet aggregation and thrombus formation. Collectively, we provide documentation that low dose of THS exposure is detrimental to health by increasing the risk of thrombosis through a hyperactive platelet phenotype that involves the toxicant NNK.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10679"},"PeriodicalIF":2.7,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13017683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573107","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":"Global MyoG research 2004-2024: a bibliometric analysis of trends and translational implications.","authors":"Luoming Hu, Weizhong Zhuang, Weimin Chen, Song Yang, Shuo Chen, Xin Wang, Qiang Gao, Jimei Chen","doi":"10.3389/ebm.2026.10929","DOIUrl":"https://doi.org/10.3389/ebm.2026.10929","url":null,"abstract":"<p><p>Myogenin (MyoG) is a core myogenic transcription factor that orchestrates myoblast differentiation and myofiber maturation and has been increasingly implicated in skeletal muscle degeneration and rhabdomyosarcoma, yet its global research landscape has not been systematically characterized. In this study, we performed a bibliometric analysis of MyoG-related publications from 2004 to 2024 retrieved from the Web of Science Core Collection. A total of 402 articles authored by 2,402 researchers from 1,148 institutions across 165 countries and regions were analyzed using VOSviewer, CiteSpace and R-based bibliometric tools. We quantified annual publication output, identified leading countries, institutions, authors and journals, and reconstructed collaboration, co-citation and keyword co-occurrence networks to delineate thematic evolution. The global pattern showed a multipolar structure dominated by the United States and China, with European institutions forming an additional hub and emerging countries contributing with growing but comparatively lower impact. Research hotspots exhibited a clear progression from early work on molecular mechanisms (DNA binding, MyoD family interactions, chromatin remodelling) toward regenerative biology (satellite cell regulation, muscle regeneration) and, more recently, disease-oriented studies focused on muscle atrophy, Duchenne muscular dystrophy and rhabdomyosarcoma. Landmark co-cited studies established MyoG as an indispensable regulator of skeletal muscle differentiation and highlighted its expanding relevance in pathological remodelling and therapeutic targeting. Future work is expected to concentrate on decoding MyoG-centred regulatory networks in degenerative muscle disease, integrating single-cell and spatial transcriptomics with functional genomics and multi-omics, and developing MyoG-based diagnostic and targeted therapeutic strategies. Despite the intrinsic limitations of single-database and citation-based approaches, this study provides a panoramic overview of two decades of MyoG research and offers a structured framework to guide future basic and translational investigations in muscle biology and oncology.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10929"},"PeriodicalIF":2.7,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12999542/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147497886","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}