American Journal of Pathology最新文献

PEX16 absence-associated hepatocyte proliferation is mediated by FXR but suppressed by PPARα. PEX16缺失相关的肝细胞增殖由FXR介导，但被PPARα抑制。

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-13 DOI: 10.1016/j.ajpath.2026.10.002

Xue Chen, Anna Mazur, Krista L Denning, George K Acquaah-Mensah, Thao Thi Nguyen, Wei Xu, Long Wang, Zhongjiao Chen, Maafi R Islam, Wei Li, William Galloway, Jun Fan, James Denvir, Logan Marshall Lawrence, Trudy Atuahene, Subha Arthur, Abdelnaby Khalyfa, Xiaodong Wang, Yongke Lu

{"title":"PEX16 absence-associated hepatocyte proliferation is mediated by FXR but suppressed by PPARα.","authors":"Xue Chen, Anna Mazur, Krista L Denning, George K Acquaah-Mensah, Thao Thi Nguyen, Wei Xu, Long Wang, Zhongjiao Chen, Maafi R Islam, Wei Li, William Galloway, Jun Fan, James Denvir, Logan Marshall Lawrence, Trudy Atuahene, Subha Arthur, Abdelnaby Khalyfa, Xiaodong Wang, Yongke Lu","doi":"10.1016/j.ajpath.2026.10.002","DOIUrl":"https://doi.org/10.1016/j.ajpath.2026.10.002","url":null,"abstract":"Peroxisomal β-oxidation processes substrate that mitochondria can't handle. For example, C27 bile acid intermediates are subjected to β-oxidation to form C24 bile acids in peroxisomes rather than in mitochondria. Peroxisome proliferation is regulated by peroxisome proliferator-activated receptor α (PPARα), which is mediated by peroxisome membrane protein PEX16. Hepatocyte-specific PEX16-deficient (Pex16Alb-Cre) mice have an upregulated PPARα signaling and display hepatocyte proliferation. It is unclear how hepatocytes proliferate in Pex16Alb-Cre mice. In this study, we treated Pex16Alb-Cre mice with PPARα agonist WY-14,643 and intestinal bile acid sequestrant cholestyramine. In addition to these pharmacological interventions, Pex16Alb-Cre mice were subjected to abrogation of PPARα and farnesoid X receptor (FXR) by crossing with PPARα-absent mice and FXR-absent mice, respectively. The results showed that WY-14,643 did not further increase hepatocyte proliferation in Pex16Alb-Cre mice, but PPARα-absent Pex16Alb-Cre mice (Pparα-/-/Pex16Alb-Cre) exhibited increased hepatocyte proliferation. In contrast, FXR-absent Pex16Alb-Cre mice (FXR-/-/Pex16Alb-Cre) displayed reduced hepatocyte proliferation. Bile acids are FXR agonists. Consistently, serum bile acids are elevated in Pex16Alb-Cre mice, and feeding cholestyramine decreased serum bile acids and inhibited hepatocyte proliferation in Pex16Alb-Cre mice. These results suggest that hepatocyte proliferation in Pex16Alb-Cre mice is mediated by FXR but inhibited by PPARα.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neutrophils drive pancreatic inflammation and tissue injury but promote tissue repair in severe acute pancreatitis. 中性粒细胞驱动胰腺炎症和组织损伤，但促进严重急性胰腺炎的组织修复。

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-13 DOI: 10.1016/j.ajpath.2026.09.008

Xiuli Zhang, Xiangyu Chen, Xiaoyu Guo, Rujuan Liu, Sohail Husain, Yun Long, Li Wen

{"title":"Neutrophils drive pancreatic inflammation and tissue injury but promote tissue repair in severe acute pancreatitis.","authors":"Xiuli Zhang, Xiangyu Chen, Xiaoyu Guo, Rujuan Liu, Sohail Husain, Yun Long, Li Wen","doi":"10.1016/j.ajpath.2026.09.008","DOIUrl":"https://doi.org/10.1016/j.ajpath.2026.09.008","url":null,"abstract":"Severe acute pancreatitis (SAP) has no targeted therapeutic options, largely owing to incomplete understanding of the mechanisms governing the transition from tissue injury to repair. Neutrophils are central effectors of sever acute pancreatitis, but their temporal contribution to injury and repair remains unresolved. Neutrophil depletion was therefore timed to defined disease stages using ROSA26iDTR/MRP8-Cre mice, in which diphtheria toxin administration was initiated on day 0, day 1, or day 2 after caerulein-induced pancreatitis; depletion efficiency was confirmed by flow cytometry. Depletion initiated on day 0 (early injury phase) reduced pancreatic injury on day 2, and histological recovery from day 4 to day 8 was more complete than in controls, a difference best explained by a reduced initial damage burden rather than a direct effect on the repair program. Depletion initiated on day 1 (late injury phase) altered neither injury nor recovery. In contrast, depletion initiated on day 2 (regenerative phase) impaired repair, with persistent acinar-to-ductal metaplasia, prolonged CD45+ infiltration, and expansion of CD86+ cells (pro-inflammatory macrophages). Neutrophils therefore function sequentially as mediators of early pancreatic injury and as required contributors to subsequent resolution, supporting that neutrophil-directed therapy should be timed to suppress pathogenic activity while preserving repair.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

TNF Receptor-2 Drives Tumoural Coagulation Factor Synthesis and Enhances Thrombosis in Clear Cell Renal Cell Carcinoma. 肿瘤坏死因子受体-2驱动肿瘤凝血因子合成并增强透明细胞肾癌血栓形成

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-13 DOI: 10.1016/j.ajpath.2026.09.006

Rafia S Al-Lamki, Jun Wang, Thomas Willingham, Jordan S Pober, Aviva M Tolkovsky, John R Bradley

{"title":"TNF Receptor-2 Drives Tumoural Coagulation Factor Synthesis and Enhances Thrombosis in Clear Cell Renal Cell Carcinoma.","authors":"Rafia S Al-Lamki, Jun Wang, Thomas Willingham, Jordan S Pober, Aviva M Tolkovsky, John R Bradley","doi":"10.1016/j.ajpath.2026.09.006","DOIUrl":"https://doi.org/10.1016/j.ajpath.2026.09.006","url":null,"abstract":"Clear-cell renal cell carcinoma (ccRCC), the most prevalent form of kidney cancer, is associated with an increased risk of local and systemic thromboembolism and a worse prognosis. The mechanisms that drive the coagulation program in tumours are not known. Combining RNAscope with immunofluorescence, local transcription of the key coagulation factors X and V, as well as prothrombin and fibrinogen chains (α, β, γ), across tumour cells, vascular endothelial cells and T cells is significantly enhanced in ccRCC tumours compared to adjacent normal kidney tissue. Elevated intratumoural protein expression of factors X and V is accompanied by local thrombin generation, fibrin deposition, and the presence of intravascular microthrombi, which themselves harbour coagulation transcripts. Mechanistic analysis using ccRCC organ cultures reveal that selective engagement of tumour necrosis factor receptor-2 (TNFR2) by a R2TNF mutein is sufficient to significantly enhance the transcription and protein expression of the same coagulation program in tumour cells, endothelial cells, and T cells compared to adjacent normal kidney cultures, whereas TNFR2 knockdown attenuates this response. In addition, TNFR2 appears to link inflammatory signalling with activation of the local coagulation system through the PI3K/Akt/MEK/NFκB signalling axes. These data provide evidence that locally produced coagulation factors driven by TNFR2 signalling may contribute to intratumoural pro-thrombotic outcomes in ccRCC, highlighting a novel pathway with potential therapeutic relevance.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Link between Activation of Lens Resident Immune Cells and Recruitment of Immune Cells to the Lens Capsule Surface in Response to Induction of EAU. EAU诱导下晶状体囊表面免疫细胞募集与晶状体驻留免疫细胞活化的关系

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-13 DOI: 10.1016/j.ajpath.2026.09.007

JodiRae DeDreu, Caitlin M Logan, Mary J Mattapallil, Rachel R Caspi, Mary Ann Stepp, A Sue Menko

{"title":"The Link between Activation of Lens Resident Immune Cells and Recruitment of Immune Cells to the Lens Capsule Surface in Response to Induction of EAU.","authors":"JodiRae DeDreu, Caitlin M Logan, Mary J Mattapallil, Rachel R Caspi, Mary Ann Stepp, A Sue Menko","doi":"10.1016/j.ajpath.2026.09.007","DOIUrl":"https://doi.org/10.1016/j.ajpath.2026.09.007","url":null,"abstract":"In Experimental Autoimmune Uveitis (EAU) mice, immune cells with an immunoregulatory phenotype are recruited to the surface of the avascular lens, traveling across ciliary zonule fibrils from the vasculature-rich ciliary body. It was also discovered that the lens epithelium harbors a population of tissue resident immune cells, a cell type associated with inducing immune responses in response to danger signals in their environment, including recruitment of immune cells that function in immune surveillance and resolution of inflammation. In this study, we examine the phenotype and localization of Lens Resident Immune Cells (LR-IC), quantify their presence in adult mouse lenses and investigate whether there is a relationship between recruitment of Lens Capsule Associated Immune Cells (LCA-ICs) and the activation of LR-ICs in EAU. This study focused on the time-period between induction of uveitis and the height of inflammation in the eyes of EAU mice. High-resolution confocal microscopy was performed on mouse eyes immunolabeled for molecules that detect activated resident immune cells or LCA-ICs. Quantification revealed that few LCA-ICs are recruited to the lens surface prior to the height of EAU inflammation, with the correlation between recruitment of immune cells to the lens capsule surface and the activation of LR-ICs occurring at the height of inflammation. These findings suggest LR-IC activation may contribute to regulation of inflammatory responses in the eye.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Direct stimulation of Ephrin-B1 induces calcium-independent podocyte injury through Cdc42-calcineurin activation. 直接刺激Ephrin-B1可通过活化cdc42钙调磷酸酶诱导钙依赖性足细胞损伤。

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-13 DOI: 10.1016/j.ajpath.2026.10.001

Yoshiyasu Fukusumi, Ying Zhang, Hidenori Yasuda, Mutsumi Kayaba, Hiroshi Kawachi

{"title":"Direct stimulation of Ephrin-B1 induces calcium-independent podocyte injury through Cdc42-calcineurin activation.","authors":"Yoshiyasu Fukusumi, Ying Zhang, Hidenori Yasuda, Mutsumi Kayaba, Hiroshi Kawachi","doi":"10.1016/j.ajpath.2026.10.001","DOIUrl":"https://doi.org/10.1016/j.ajpath.2026.10.001","url":null,"abstract":"Although a subset of nephrotic syndrome has been reported to be caused by autoantibodies against nephrin, its etiology remains poorly understood. A previous study demonstrated that anti-nephrin antibodies phosphorylate not only nephrin but also Ephrin-B1 at the slit diaphragm of podocytes. However, the pathogenic role of Ephrin-B1 in nephrotic syndrome remains unclear. The present study, using cultured human podocytes, demonstrated that direct stimulation of Ephrin-B1 with soluble EphB2 or an anti-Ephrin-B1 antibody induced phosphorylation of both Ephrin-B1 and nephrin. Neither EphB2 nor the anti-Ephrin-B1 antibody induced calcium influx, whereas the anti-nephrin antibody did. Phosphorylated Ephrin-B1 dissociated from Par6, and the released Par6 subsequently interacted with Cdc42. This interaction promoted Cdc42 activation, leading to altered regulation of Snail and STAT3. These alterations resulted in decreased expression of nephrin and Ephrin-B1 and induced claudin-1 expression. A Cdc42 inhibitor prevented both the downregulation of nephrin and Ephrin-B1 and the induction of claudin-1 expression. In contrast, a calcineurin inhibitor and an angiotensin II type 1 receptor blocker prevented the downregulation of nephrin and Ephrin-B1 but failed to prevent claudin-1 induction. This study proposed a novel potential etiology of nephrotic syndrome caused by direct stimulation of Ephrin-B1. Targeting Cdc42 may represent a more effective therapeutic strategy for restoring podocyte homeostasis.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149178614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Foundation Model-Based Computational Pathology Predicts Breast Cancer Biomarker Status from Intraoperative Frozen Sections. 基于基础模型的计算病理学预测术中冷冻切片的乳腺癌生物标志物状态。

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-05 DOI: 10.1016/j.ajpath.2026.09.005

Shun Liu, Jun Li, Yixiang Lian, Jie Lan, Tingyu Zhang, Huiru He, Meng Du, Haijun Luo, Zhiyi Chen

{"title":"Foundation Model-Based Computational Pathology Predicts Breast Cancer Biomarker Status from Intraoperative Frozen Sections.","authors":"Shun Liu, Jun Li, Yixiang Lian, Jie Lan, Tingyu Zhang, Huiru He, Meng Du, Haijun Luo, Zhiyi Chen","doi":"10.1016/j.ajpath.2026.09.005","DOIUrl":"10.1016/j.ajpath.2026.09.005","url":null,"abstract":"Prediction of breast cancer biomarkers from routine formalin-fixed, paraffin-embedded (FFPE) hematoxylin and eosin (H&E) images has been explored previously, but whether biomarker-associated morphologic signals can be reliably captured from artifact-prone intraoperative frozen-section (FS) specimens remains insufficiently studied. This retrospective proof-of-concept study developed a foundation model-based multiple-instance learning framework to predict estrogen receptor (ER), progesterone receptor (PR), human epidermal growth factor receptor 2 (HER2), and Ki-67 status directly from H&E-stained intraoperative FS whole slide images of 248 patients with breast cancer, using postoperative immunohistochemistry and fluorescence in situ hybridization as ground truth. Exploratory feature evaluation identified UNI2-h as a suitable encoder for downstream modeling. In fivefold cross-validation, areas under the receiver operating characteristic curve were 0.847 for ER, 0.906 for PR, 0.893 for HER2, and 0.799 for Ki-67, with moderate agreement for ER, PR, and HER2 and fair agreement for Ki-67. An exploratory within-cohort cross-preparation analysis showed limited FFPE-to-FS transferability, whereas the FS-trained model retained relatively favorable performance on FFPE images. Attention heat maps highlighted tumor regions with biologically plausible biomarker-associated morphologic patterns. These findings provide proof of concept that intraoperative FS H&E images retain learnable biomarker-associated morphologic signals despite preparation-related alterations.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Multi-Omic Analysis of Peripheral Circulating Neutrophils and the Effects of Transmigration. 外周循环中性粒细胞的多组学分析及其转运的影响。

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-03 DOI: 10.1016/j.ajpath.2026.08.010

Laura C Morales, Anjelica L Gonzalez

{"title":"Multi-Omic Analysis of Peripheral Circulating Neutrophils and the Effects of Transmigration.","authors":"Laura C Morales, Anjelica L Gonzalez","doi":"10.1016/j.ajpath.2026.08.010","DOIUrl":"10.1016/j.ajpath.2026.08.010","url":null,"abstract":"Neutrophils, the most prevalent leukocytes in circulation, are integral to initiating and resolving inflammatory responses. Although traditionally viewed as a homogeneous population, emerging studies have revealed significant phenotypic heterogeneity and functional versatility within the neutrophil population. However, developing a consensus on neutrophil markers for precise and comprehensive identification of neutrophil phenotypes at baseline is essential to deepen understanding of their biology. In this study, a combination of single-cell RNA sequencing and advanced multiplex flow cytometry analyses was used to examine the transcriptional and proteomic landscapes of human neutrophils in healthy peripheral blood while using functional assays to assess their migratory capabilities and phenotypic alterations after transmigration. Through transcriptional and proteomic analyses, the findings identify three distinct neutrophil profiles, each characterized by specific effector functions and migratory patterns. These subsets demonstrated distinction in the expression of markers related to neutrophil maturation, aging, immune modulation, and inflammatory responses, suggesting a complex spectrum of neutrophil states in circulation and after vascular transmigration. The findings advance the field's understanding of neutrophil heterogeneity and offer a more nuanced view of their roles in homeostasis and the immune response.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149103053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Title Page 标题页

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-01 Epub Date: 2026-10-17 DOI: 10.1016/S0002-9440(26)00291-9

引用次数: 0

Meeting Abstracts 会议摘要

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-10-01 Epub Date: 2026-10-17 DOI: 10.1016/j.ajpath.2026.10.003

引用次数: 0

Wnt/β-Catenin Reduces Fibrosis and Enhances Hepatocyte Reprogramming during Cholestasis Independent of Yes-Associated Protein Signaling. Wnt/β-catenin在不依赖于Yap信号的胆汁淤滞期间减少纤维化并增强肝细胞重编程。

IF 4.9 2区医学

American Journal of Pathology Pub Date : 2026-09-25 DOI: 10.1016/j.ajpath.2026.09.003

Veronica Lee, Chun-Cheng Chiang, Oluwashanu Balogun, Pamela Cornuet, Matthew Carson, Rithwik Aggarwal, Ridgeway H Case, Chhavi Goel, Salma O El-Mossier, Jia-Jun Liu, Silvia Liu, Kari Nejak-Bowen

{"title":"Wnt/β-Catenin Reduces Fibrosis and Enhances Hepatocyte Reprogramming during Cholestasis Independent of Yes-Associated Protein Signaling.","authors":"Veronica Lee, Chun-Cheng Chiang, Oluwashanu Balogun, Pamela Cornuet, Matthew Carson, Rithwik Aggarwal, Ridgeway H Case, Chhavi Goel, Salma O El-Mossier, Jia-Jun Liu, Silvia Liu, Kari Nejak-Bowen","doi":"10.1016/j.ajpath.2026.09.003","DOIUrl":"10.1016/j.ajpath.2026.09.003","url":null,"abstract":"Cholestatic liver diseases are characterized by impaired bile flow. Repairing damage and reestablishing biliary function may slow disease progression and reduce complications. The Wnt/β-catenin pathway can facilitate biliary repair during cholestasis through multiple mechanisms. The impact of constitutive Wnt/β-catenin signaling during cholestasis was analyzed using S45D transgenic (TG) mice, which express nondegradable β-catenin. Compared with wild type (WT), TG mice had increased inflammation and decreased fibrosis during prolonged cholestasis. Furthermore, TG mice had increased ductular reaction and hepatocyte reprogramming, which may alleviate injury. Because both Wnt/β-catenin and Yes-associated protein (Yap) pathways are implicated in cell plasticity, whether β-catenin works in concordance with or independent of Yap was investigated. In vitro studies demonstrated that Yap was not required for Wnt-mediated hepatocyte reprogramming. Spatial transcriptomics demonstrated suppression of Wnt/β-catenin activity in pericentral hepatocytes, whereas periportal Yap activation increased in early cholestasis. A dual reporter mouse model showed enhanced Wnt activation in both pericentral and periportal TG HC compared with WT, whereas Yap activation was equivalent in WT and TG. Transcriptomic analysis of human livers demonstrated that Wnt/β-catenin and Yap target genes also map to distinct cell compartments in cholestatic patients. These findings suggest that enhanced Wnt/β-catenin activation in TG mice accelerates compensatory responses and attenuates disease progression. Activation of Wnt/β-catenin and Yap in different cell types indicates that β-catenin functions independently of Yap.","PeriodicalId":7623,"journal":{"name":"American Journal of Pathology","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0