Hereditas最新文献

{"title":"Development and implementation of an etiology-based diagnostic framework for acute abdominal pain in emergency settings.","authors":"Hui Guo, Xu-Rui Li, Yun-Lei Du, Yang-Juan Jia, Hong-Ling Li, Qian Zhao, Yan-Peng Li, Jian-Guo Li","doi":"10.1186/s41065-025-00507-3","DOIUrl":"10.1186/s41065-025-00507-3","url":null,"abstract":"<p><strong>Background: </strong>Diagnostic checklists have been demonstrated to reduce errors in clinical reasoning. Building on previous validation studies, this research presents the development and clinical application of an etiology-based diagnostic framework for evaluating acute abdominal pain. The framework integrates a structured checklist of abdominal pain etiologies with a process-oriented diagnostic strategy, aiming to enhance diagnostic accuracy and clinical outcomes. This approach also serves as a potential model for the creation of diagnostic tools applicable to other symptom complexes encountered in emergency medicine.</p><p><strong>Methods: </strong>A cognitive task analysis (CTA) was conducted with participation from five emergency medicine experts employing a think-aloud methodology. The experts described their diagnostic reasoning processes and queried relevant clinical data to extract foundational diagnostic principles. Based on these findings, a checklist categorizing etiologies of abdominal pain was constructed, drawing from anatomical and diagnostic considerations. The clinical utility of the checklist was evaluated through its application to a representative complex case.</p><p><strong>Results: </strong>The diagnostic checklist was organized into five principal etiological categories: local organ disorders, diseases of adjacent organs, systemic diseases, psychogenic disorders, and gynecological conditions. Its implementation facilitated the accurate identification of atypical acute renal infarction in a diagnostically challenging case, enabling prompt clinical intervention.</p><p><strong>Conclusions: </strong>CTA provides a robust method for modeling expert diagnostic reasoning and supports the development of structured, etiology-based diagnostic tools. This framework enhances diagnostic precision for individuals presenting with acute abdominal pain in emergency settings and may inform the development of similar tools for other clinical presentations.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"134"},"PeriodicalIF":2.7,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM15 promotes hypoxia/reoxygenation-induced ferroptosis in human cardiomyocytes by mediating m6A modification of ACSL4.","authors":"Yi Cheng, Jiamin Wan, Yingyue Xu, Shasha Liu, Linfeng Li, Jing Zhou, Fuyan Xie","doi":"10.1186/s41065-025-00453-0","DOIUrl":"10.1186/s41065-025-00453-0","url":null,"abstract":"<p><strong>Background: </strong>Acute myocardial infarction (AMI) refers to the acute necrosis of part of the myocardium caused by persistent and severe myocardial ischemia. The aim of the study was to investigate the effect of RNA binding motif protein 15 (RBM15) and acyl-CoA synthetase long chain family member 4 (ACSL4) on ischemia/reperfusion (I/R)-induced ferroptosis of cardiomyocytes.</p><p><strong>Methods and results: </strong>AC16 cells were treated with hypoxia/reoxygenation (H/R) to establish an in vitro myocardial infarction cell model. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay were used to determine gene expression. Cell Counting Kit-8 (CCK-8) assay was conducted to investigate cell viability. Ferroptosis level was evaluated by commercial kits. N6-methyladenosine (m6A) level was examined by M6A quantification analysis. RNA immunoprecipitation (RIP) assay, methylated RNA Immunoprecipitation (meRIP) assay and dual-luciferase reporter assay were adopted to verify the combination between RBM15 and ACSL4. ACSL4 mRNA stability was analyzed by Actinomycin D treatment. RBM15 mRNA level was increased in AMI patients' serums and H/R-induced AC16 cells. Silencing of RBM15 promoted H/R-mediated AC16 cell viability and inhibited H/R-induced AC16 cell oxidative stress and ferroptosis. Moreover, it was demonstrated that RBM15 knockdown inhibited m6A modification of ACSL4 and suppressed the stability of ACSL4 mRNA. Furthermore, ACSL4 overexpression restored the effects of RNM15 silencing on H/R-induced AC16 cell oxidative injury and ferroptosis.</p><p><strong>Conclusion: </strong>RBM15 silencing repressed H/R-induced ferroptosis in human cardiomyocytes through regulating m6A modification of ACSL4.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"135"},"PeriodicalIF":2.7,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing LncRNA HCG27 ameliorates cognitive dysfunction after ischemic stroke via miR-27a-3p regulation.","authors":"Ting Li, Ying Li, Lin Chen, Chaosheng Zeng, Huaijie Xing, Min Chen, Limin Yan, Xiaopei Zhang","doi":"10.1186/s41065-025-00493-6","DOIUrl":"10.1186/s41065-025-00493-6","url":null,"abstract":"<p><strong>Background: </strong>We explore the effect of improving cognitive dysfunction after cerebral ischemia-reperfusion (CI/R) by regulating HCG27.</p><p><strong>Methods: </strong>The MCAO and OGD/R methods were employed to establish in vivo and in vitro models of cognitive dysfunction caused by a CI/R injury. RT-qPCR was utilized to detect the relative expression of HCG27 and miR-27a-3p. An ELISA was adopted to measure the concentrations of inflammatory factors (IL-6, IL-1β, IL-10). The concentration of MDA and activity of CAT were detected using commercially available kits. The neurological deficit was evaluated using the mNSS score. The spatial learning and memory capabilities were evaluated via the MWM test. The targeting relationships were validated by the dual-luciferase reporter assay, RIP assay, and RNA pull-down assay. The CCK-8 assay and flow cytometry were employed to asses cell viability and apoptosis, respectively.</p><p><strong>Results: </strong>The level of HCG27 was upregulated in MCAO rats and OGD/R-induced BV2 cells, whereas that of miR-27a-3p decreased, and HCG27 targeted miR-27a-3p. Compared with the sham group, the mNSS score of MCAO rats was elevated, and their spatial learning and memory abilities declined, with aggravated inflammatory response and oxidative stress. However, silencing HCG27 improved these conditions, and the miR-27a-3p antagonist reversed this. MiR-27a-3p reversed the increase in cell viability in OGD/R-induced BV2 cells, reduced the cell apoptosis rate, and weakened the inflammatory response and oxidative stress caused by the HCG27 silencing.</p><p><strong>Conclusions: </strong>Silencing HCG27 can protect against cognitive dysfunction after cerebrovascular disease by targeting miR-27a-3p.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"136"},"PeriodicalIF":2.7,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12275291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of miR-107/HMOX1 axis in hepatic sinusoidal endothelial cells stimulated by ischemia-reperfusion injury.","authors":"Zhao Wang, Jiangyang Sun, Yu Wang, Yichuan Zhang, Laian Ge","doi":"10.1186/s41065-025-00495-4","DOIUrl":"10.1186/s41065-025-00495-4","url":null,"abstract":"<p><strong>Background: </strong>Liver ischemia-reperfusion injury (IRI) is a common complication of diseases such as liver transplantation, hepatic resection, and hemorrhagic shock. This study aimed to elucidate the molecular mechanism of miR-107 affecting hepatic ischemia-reperfusion injury (IRI).</p><p><strong>Methods: </strong>The expression changes of miR-107 during hepatic IRI were quantified using quantitative real-time PCR. Subsequently, in vitro cellular experiments were carried out to verify the role of miR-107 on hypoxia/reoxygenation (HR) through CCK-8, flow cytometer, and commercial kits. In terms of mechanism, it was determined that miR-107 had a regulatory relationship with target genes through luciferase reporter assay.</p><p><strong>Results: </strong>In mouse liver IRI, miR-107 expression was increased while HMOX1 expression was decreased in liver tissues. In vitro cellular experiments, miR-107 inhibitors favored the alleviation of proliferation, apoptosis, inflammation, and oxidative stress in HR-damaged liver sinusoidal endothelial cells. In the molecular mechanism study, we determined that miR-107 could bind to HMOX1 and inhibit the HMOX1 expression. Low HMOX1 expression could eliminate the protective effect of miR-107 inhibitors.</p><p><strong>Conclusion: </strong>MiR-107 expression was elevated during hepatic IRI and exacerbates hepatic injury by targeting HMOX1 inhibition.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"133"},"PeriodicalIF":2.7,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delving into the pinnacle: an in-depth analysis of the top 100 most cited articles on cardio-oncology.","authors":"Ping Lai, Shuquan Xu, Zi-Xuan Cao, Zi-You Liu, Ke-Jun Tian, Wen-Ting Zhong, Xia Liu, Yi-Ming Zhong, Xiao-Ping Wang, Jin-Hua Xue","doi":"10.1186/s41065-025-00497-2","DOIUrl":"10.1186/s41065-025-00497-2","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"132"},"PeriodicalIF":2.7,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ulnar nerve entrapment syndrome: a special case report.","authors":"Yifeng Han, Dachuan Sun, Mao Ye, Xindong Fan, Jiaxue Zhu","doi":"10.1186/s41065-025-00506-4","DOIUrl":"10.1186/s41065-025-00506-4","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"130"},"PeriodicalIF":2.7,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in enhanced recovery after surgery (ERAS) in thoracic surgery from a bibliometric insight.","authors":"Yafeng Liu, Tianze Zhang, Tong Gao, Guanghua Li, Guangquan Xu","doi":"10.1186/s41065-025-00501-9","DOIUrl":"10.1186/s41065-025-00501-9","url":null,"abstract":"<p><strong>Background: </strong>In thoracic surgery, the concept of Enhanced Recovery After Surgery (ERAS) has been extensively implemented. Although numerous studies have investigated ERAS in thoracic surgery, bibliometric analyses remain limited. In this study, the developmental trajectory, current research status, and prospective trends of ERAS in thoracic surgery were systematically analyzed through bibliometric and visual analysis techniques.</p><p><strong>Methods: </strong>Literature pertaining to ERAS in thoracic surgery was retrieved from the Web of Science Core Collection (WoSCC). Microsoft Excel 2019, R software (version 4.1.0), the Bibliometric Online Analysis Platform, VOSviewer (version 1.6.18), and Citespace (version 6.3.R1) were utilized for statistical analysis, bibliometric evaluation, and data visualization.</p><p><strong>Results: </strong>A total of 617 publications were retrieved over the past decade. The number of publications has generally demonstrated an upward trend from 2015 to 2024. China and Sichuan University ranked as the leading country and institution, respectively, in terms of publication volume. The Journal of Thoracic Disease was identified as the leading journal in both publication count and citation frequency. Henrik Kehlet was recognized as the most prolific and highly co-cited author. Current research hotspots include \"video-assisted thoracic surgery,\" \"pain management,\" and \"multicenter clinical trials.\"</p><p><strong>Conclusion: </strong>ERAS-related research in thoracic surgery has been increasing steadily, highlighting it as a rapidly evolving and promising field. The ERAS concept plays a critical role in all perioperative phases-preoperative, intraoperative, and postoperative-and requires further in-depth investigation. Many existing ERAS studies in thoracic surgery lack high-quality evidence, underscoring the urgent need for rigorously designed research with robust methodological standards.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"131"},"PeriodicalIF":2.7,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High tidal volume mechanical ventilation exacerbates pulmonary injury via upregulation of PAI-1 expression in rats.","authors":"Jun-Ming Ren, Gui-Fei Wang, Jing Bi, Zhi Wang, Wei-Wei Zhang","doi":"10.1186/s41065-025-00446-z","DOIUrl":"10.1186/s41065-025-00446-z","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the impact of different mechanical ventilation strategies on pulmonary plasminogen activator inhibitor-1 (PAI-1) expression in a rat model.</p><p><strong>Methods: </strong>Seventy-two specific pathogen-free (SPF) adult male Sprague-Dawley (SD) rats were randomly assigned to four groups (n = 18): Group C (spontaneous breathing), group S (low tidal volume, VT = 6 mL/kg), group R (regular tidal volume, VT = 10 mL/kg), and group L (high tidal volume, VT = 40 mL/kg). Each group was further divided into three subgroups based on mechanical ventilation duration (2, 4, or 6 h). Following tracheotomy intubation, group C maintained spontaneous breathing, while the other groups underwent mechanical ventilation with a small animal ventilator. Lung wet-to-dry weight ratios, cell apoptosis rate, and lung injury score were recorded. PAI-1 and IL-8 levels were measured in bronchoalveolar lavage fluid (BALF), and PAI-1 mRNA expression in lung tissue was analyzed using real-time polymerase chain reaction (PCR).</p><p><strong>Results: </strong>Progressive lung tissue injury was observed in Group L with increasing ventilation durations, accompanied by significant increases in PAI-1, IL-8, and PAI-1 mRNA expression, compared to group C (P < 0.05). No significant differences were identified between Group S and group C, while group R exhibited mild lung injury and minimal increases in PAI-1 expression, observed only after 6 h of ventilation. In group L, PAI-1, IL-8, and PAI-1 mRNA expression increased significantly with extended ventilation durations (P < 0.05).</p><p><strong>Conclusion: </strong>Mechanical ventilation strategies utilizing high tidal volumes were associated with substantial increases in PAI-1 expression in rat lung tissue and BALF, with these effects exacerbated by prolonged ventilation durations. These findings suggest that high tidal volume ventilation strategies may contribute to pulmonary injury by upregulating PAI-1 expression.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"129"},"PeriodicalIF":2.7,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261637/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insight into the shared pathogenic link between COVID-19 and pterygium: a systematic bioinformatics analysis with experimental validation.","authors":"Tianyi Zhou, Xueyao Cai, Wenjun Shi, Xia Ding, Yuchen Cai","doi":"10.1186/s41065-025-00500-w","DOIUrl":"10.1186/s41065-025-00500-w","url":null,"abstract":"<p><p>The outbreak of coronavirus disease 2019 (COVID-19) has resulted in a remarkable threat to global public health over the past few years. Despite the tremendous studies of COVID-19 ongoing, few have focused on the viral impact on the ocular surface. As one of the most common inflammatory diseases of the ocular surface, pterygium could be triggered under multiple environmental exposures. In the present work, we aimed at investigating the potential interactions between pterygium and COVID-19. Based on bioinformatic tools, we compared databases of COVID-19 and pterygium and screened for common differentially expressed genes (DEGs). Multifactor regulatory network and co-expression network of the common DEGs were analyzed. In vitro experiments, including siRNA knockdown using human conjunctival fibroblasts (HConFs) confirmed the bioinformatics results. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis implied that immune response was associated with COVID-19-induced ocular events. We then identified five common DEGs, including ERP27, SYTL5, STXBP6, EXTL1 and DIO2, which was further validated by in vitro experiments. Three hub genes were further extracted which included SYTL5, STXBP6 and ERP27 through protein-protein interactions (PPI) network. Furthermore, we illustrated a regulatory network consisting of eight transcription factors (STAT6B, GATA1, POU2F2, PGR, RBPJ, STAT3, CRTC1 and HMGA1) and one microRNA (hsa-miR-384). Overall, we investigated the common link between SARS-CoV-2 and pterygium in the modulation of gene profiles on the ocular surface. Our study proposed a novel insight into the common pathogenic mechanisms between COVID-19 and pterygium, which are associated with immune dysregulation and pathological proliferation, indicating a viral impact on pterygium susceptibility. This innovative perspective may enable a more comprehensive understanding and advance towards improved clinical prevention and treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"128"},"PeriodicalIF":2.7,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12261744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced miR-338-3p contributes to polycystic ovarian syndrome by inhibiting proliferation and enhancing apoptosis.","authors":"Lin Liang, Jie Lv, Wei Li, Chengwen Song, Ying Chen, Huafang Wei","doi":"10.1186/s41065-025-00498-1","DOIUrl":"10.1186/s41065-025-00498-1","url":null,"abstract":"<p><strong>Background: </strong>Polycystic ovarian syndrome (PCOS) is a frequently occurring disorder affecting reproductive and metabolic health. miR-338-3p is implicated in early follicular development. We aimed to investigate the expression of miR-338-3p in PCOS patients and its effects on proliferation and apoptosis of ovarian granulosa cells.</p><p><strong>Methods: </strong>The study included 100 healthy women and 110 women diagnosed with PCOS as participants. Reverse transcription quantitative PCR (RT-qPCR) was used to detect the expression of miR-338-3p and phosphatase and tensin homolog (PTEN), and receiver operating characteristic (ROC) was employed to evaluate the diagnostic efficacy of miR-338-3p. Cell proliferation and apoptosis were detected by Cell Counting Kit-8 (CCK-8) and flow cytometry. Pearson correlation analysis was used to assess the correlations between miR-338-3p and luteinizing hormone (LH), testosterone, or PTEN. The target relationship of miR-338-3p and PTEN was confirmed via dual-luciferase assay.</p><p><strong>Results: </strong>Serum miR-338-3p was decreased in PCOS patients, and it was negatively correlated with both LH and testosterone. Downregulation of miR-338-3p inhibits the proliferation of ovarian granulosa cells and enhances cell apoptosis, whereas upregulation produces the opposite effect. PTEN inhibition subverted the inhibited proliferation and enhanced apoptosis regulated by miR-338-3p inhibitor.</p><p><strong>Conclusions: </strong>Reduced miR-338-3p levels have potential predictive value in distinguishing individuals with PCOS patients from normal population. Mechanistically, this microRNA regulates the PTEN gene to inhibit granulosa cell proliferation and promote apoptosis, thereby contributing to the pathological processes of PCOS.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"126"},"PeriodicalIF":2.7,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144617150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}