Frontiers of Medicine最新文献_第7页

Autophagy in hepatic progenitor cells modulates exosomal miRNAs to inhibit liver fibrosis in schistosomiasis. 肝祖细胞的自噬调节外泌体miRNA，从而抑制血吸虫病的肝纤维化。

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-06-01 Epub Date: 2024-05-21 DOI: 10.1007/s11684-024-1079-1

Yue Yuan, Jiaxuan Li, Xun Lu, Min Chen, Huifang Liang, Xiao-Ping Chen, Xin Long, Bixiang Zhang, Song Gong, Xiaowei Huang, Jianping Zhao, Qian Chen

{"title":"Autophagy in hepatic progenitor cells modulates exosomal miRNAs to inhibit liver fibrosis in schistosomiasis.","authors":"Yue Yuan, Jiaxuan Li, Xun Lu, Min Chen, Huifang Liang, Xiao-Ping Chen, Xin Long, Bixiang Zhang, Song Gong, Xiaowei Huang, Jianping Zhao, Qian Chen","doi":"10.1007/s11684-024-1079-1","DOIUrl":"10.1007/s11684-024-1079-1","url":null,"abstract":"Schistosoma infection is one of the major causes of liver fibrosis. Emerging roles of hepatic progenitor cells (HPCs) in the pathogenesis of liver fibrosis have been identified. Nevertheless, the precise mechanism underlying the role of HPCs in liver fibrosis in schistosomiasis remains unclear. This study examined how autophagy in HPCs affects schistosomiasis-induced liver fibrosis by modulating exosomal miRNAs. The activation of HPCs was verified by immunohistochemistry (IHC) and immunofluorescence (IF) staining in fibrotic liver from patients and mice with Schistosoma japonicum infection. By coculturing HPCs with hepatic stellate cells (HSCs) and assessing the autophagy level in HPCs by proteomic analysis and in vitro phenotypic assays, we found that impaired autophagy degradation in these activated HPCs was mediated by lysosomal dysfunction. Blocking autophagy by the autophagy inhibitor chloroquine (CQ) significantly diminished liver fibrosis and granuloma formation in S. japonicum-infected mice. HPC-secreted extracellular vehicles (EVs) were further isolated and studied by miRNA sequencing. miR-1306-3p, miR-493-3p, and miR-34a-5p were identified, and their distribution into EVs was inhibited due to impaired autophagy in HPCs, which contributed to suppressing HSC activation. In conclusion, we showed that the altered autophagy process upon HPC activation may prevent liver fibrosis by modulating exosomal miRNA release and inhibiting HSC activation in schistosomiasis. Targeting the autophagy degradation process may be a therapeutic strategy for liver fibrosis during Schistosoma infection.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"538-557"},"PeriodicalIF":8.1,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Progress on early diagnosing Alzheimer's disease. 早期诊断阿尔茨海默病的进展。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2024-06-01 Epub Date: 2024-05-21 DOI: 10.1007/s11684-023-1047-1

Yixin Chen, Murad Al-Nusaif, Song Li, Xiang Tan, Huijia Yang, Huaibin Cai, Weidong Le

{"title":"Progress on early diagnosing Alzheimer's disease.","authors":"Yixin Chen, Murad Al-Nusaif, Song Li, Xiang Tan, Huijia Yang, Huaibin Cai, Weidong Le","doi":"10.1007/s11684-023-1047-1","DOIUrl":"10.1007/s11684-023-1047-1","url":null,"abstract":"Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects both cognition and non-cognition functions. The disease follows a continuum, starting with preclinical stages, progressing to mild cognitive and behavioral impairment, ultimately leading to dementia. Early detection of AD is crucial for better diagnosis and more effective treatment. However, the current AD diagnostic tests of biomarkers using cerebrospinal fluid and/or brain imaging are invasive or expensive, and mostly are still not able to detect early disease state. Consequently, there is an urgent need to develop new diagnostic techniques with higher sensitivity and specificity during the preclinical stages of AD. Various non-cognitive manifestations, including behavioral abnormalities, sleep disturbances, sensory dysfunctions, and physical changes, have been observed in the preclinical AD stage before occurrence of notable cognitive decline. Recent research advances have identified several biofluid biomarkers as early indicators of AD. This review focuses on these non-cognitive changes and newly discovered biomarkers in AD, specifically addressing the preclinical stages of the disease. Furthermore, it is of importance to explore the potential for developing a predictive system or network to forecast disease onset and progression at the early stage of AD.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"446-464"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11391414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141070811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum to: Potential unreliability of ALK variant allele frequency in the efficacy prediction of targeted therapy in NSCLC. 勘误：ALK变异等位基因频率在NSCLC靶向治疗疗效预测中的潜在不可靠因素。

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-06-01 DOI: 10.1007/s11684-024-1076-4

Wei Rao, Yutao Liu, Yan Li, Lei Guo, Tian Qiu, Lin Dong, Jianming Ying, Weihua Li

引用次数: 0

Immune landscape and response to oncolytic virus-based immunotherapy. 免疫格局和对基于溶瘤病毒的免疫疗法的反应。

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2024-06-01 Epub Date: 2024-03-08 DOI: 10.1007/s11684-023-1048-0

Chaolong Lin, Wenzhong Teng, Yang Tian, Shaopeng Li, Ningshao Xia, Chenghao Huang

{"title":"Immune landscape and response to oncolytic virus-based immunotherapy.","authors":"Chaolong Lin, Wenzhong Teng, Yang Tian, Shaopeng Li, Ningshao Xia, Chenghao Huang","doi":"10.1007/s11684-023-1048-0","DOIUrl":"10.1007/s11684-023-1048-0","url":null,"abstract":"Oncolytic virus (OV)-based immunotherapy has emerged as a promising strategy for cancer treatment, offering a unique potential to selectively target malignant cells while sparing normal tissues. However, the immunosuppressive nature of tumor microenvironment (TME) poses a substantial hurdle to the development of OVs as effective immunotherapeutic agents, as it restricts the activation and recruitment of immune cells. This review elucidates the potential of OV-based immunotherapy in modulating the immune landscape within the TME to overcome immune resistance and enhance antitumor immune responses. We examine the role of OVs in targeting specific immune cell populations, including dendritic cells, T cells, natural killer cells, and macrophages, and their ability to alter the TME by inhibiting angiogenesis and reducing tumor fibrosis. Additionally, we explore strategies to optimize OV-based drug delivery and improve the efficiency of OV-mediated immunotherapy. In conclusion, this review offers a concise and comprehensive synopsis of the current status and future prospects of OV-based immunotherapy, underscoring its remarkable potential as an effective immunotherapeutic agent for cancer treatment.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"411-429"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140059108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

lncRNA ZNF593-AS inhibits cardiac hypertrophy and myocardial remodeling by upregulating Mfn2 expression. lncRNA ZNF593-AS通过上调Mfn2的表达抑制心脏肥大和心肌重塑

IF 3.9 3区医学

Frontiers of Medicine Pub Date : 2024-06-01 Epub Date: 2024-05-14 DOI: 10.1007/s11684-023-1036-4

Xiang Nie, Jiahui Fan, Yanwen Wang, Rong Xie, Chen Chen, Huaping Li, Dao Wen Wang

{"title":"lncRNA ZNF593-AS inhibits cardiac hypertrophy and myocardial remodeling by upregulating Mfn2 expression.","authors":"Xiang Nie, Jiahui Fan, Yanwen Wang, Rong Xie, Chen Chen, Huaping Li, Dao Wen Wang","doi":"10.1007/s11684-023-1036-4","DOIUrl":"10.1007/s11684-023-1036-4","url":null,"abstract":"lncRNA ZNF593 antisense (ZNF593-AS) transcripts have been implicated in heart failure through the regulation of myocardial contractility. The decreased transcriptional activity of ZNF593-AS has also been detected in cardiac hypertrophy. However, the function of ZNF593-AS in cardiac hypertrophy remains unclear. Herein, we report that the expression of ZNF593-AS reduced in a mouse model of left ventricular hypertrophy and cardiomyocytes in response to treatment with the hypertrophic agonist phenylephrine (PE). In vivo, ZNF593-AS aggravated pressure overload-induced cardiac hypertrophy in knockout mice. By contrast, cardiomyocyte-specific transgenic mice (ZNF593-AS MHC-Tg) exhibited attenuated TAC-induced cardiac hypertrophy. In vitro, vector-based overexpression using murine or human ZNF593-AS alleviated PE-induced myocyte hypertrophy, whereas GapmeR-induced inhibition aggravated hypertrophic phenotypes. By using RNA-seq and gene set enrichment analyses, we identified a link between ZNF593-AS and oxidative phosphorylation and found that mitofusin 2 (Mfn2) is a direct target of ZNF593-AS. ZNF593-AS exerts an antihypertrophic effect by upregulating Mfn2 expression and improving mitochondrial function. Therefore, it represents a promising therapeutic target for combating pathological cardiac remodeling.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"484-498"},"PeriodicalIF":3.9,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140921593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Identification of a novel MYO1D variant associated with laterality defects, congenital heart diseases, and sperm defects in humans 鉴定与人类侧位缺陷、先天性心脏病和精子缺陷有关的新型 MYO1D 变异基因

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-04-30 DOI: 10.1007/s11684-023-1042-6

Zhuangzhuang Yuan, Xin Zhu, Xiaohui Xie, Chenyu Wang, Heng Gu, Junlin Yang, Liangliang Fan, Rong Xiang, Yifeng Yang, Zhiping Tan

{"title":"Identification of a novel MYO1D variant associated with laterality defects, congenital heart diseases, and sperm defects in humans","authors":"Zhuangzhuang Yuan, Xin Zhu, Xiaohui Xie, Chenyu Wang, Heng Gu, Junlin Yang, Liangliang Fan, Rong Xiang, Yifeng Yang, Zhiping Tan","doi":"10.1007/s11684-023-1042-6","DOIUrl":"https://doi.org/10.1007/s11684-023-1042-6","url":null,"abstract":"The establishment of left–right asymmetry is a fundamental process in animal development. Interference with this process leads to a range of disorders collectively known as laterality defects, which manifest as abnormal arrangements of visceral organs. Among patients with laterality defects, congenital heart diseases (CHD) are prevalent. Through multiple model organisms, extant research has established that myosin-Id (MYO1D) deficiency causes laterality defects. This study investigated over a hundred cases and identified a novel biallelic variant of MYO1D (NM_015194: c.1531G>A; p.D511N) in a consanguineous family with complex CHD and laterality defects. Further examination of the proband revealed asthenoteratozoospermia and shortened sperm. Afterward, the effects of the D511N variant and another known MYO1D variant (NM_015194: c.2293C>T; p.P765S) were assessed. The assessment showed that both enhance the interaction with β-actin and SPAG6. Overall, this study revealed the genetic heterogeneity of this rare disease and found that MYO1D variants are correlated with laterality defects and CHD in humans. Furthermore, this research established a connection between sperm defects and MYO1D variants. It offers guidance for exploring infertility and reproductive health concerns. The findings provide a critical basis for advancing personalized medicine and genetic counseling.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":"52 1","pages":""},"PeriodicalIF":8.1,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140829979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Targeting deubiquitinase OTUB1 protects vascular smooth muscle cells in atherosclerosis by modulating PDGFRβ 以去泛素化酶 OTUB1 为靶标，通过调节 PDGFRβ 保护动脉粥样硬化中的血管平滑肌细胞

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-04-22 DOI: 10.1007/s11684-024-1056-8

Fei Xu, Han Chen, Changyi Zhou, Tongtong Zang, Rui Wang, Shutong Shen, Chaofu Li, Yue Yu, Zhiqiang Pei, Li Shen, Juying Qian, Junbo Ge

{"title":"Targeting deubiquitinase OTUB1 protects vascular smooth muscle cells in atherosclerosis by modulating PDGFRβ","authors":"Fei Xu, Han Chen, Changyi Zhou, Tongtong Zang, Rui Wang, Shutong Shen, Chaofu Li, Yue Yu, Zhiqiang Pei, Li Shen, Juying Qian, Junbo Ge","doi":"10.1007/s11684-024-1056-8","DOIUrl":"https://doi.org/10.1007/s11684-024-1056-8","url":null,"abstract":"Atherosclerosis is a chronic artery disease that causes various types of cardiovascular dysfunction. Vascular smooth muscle cells (VSMCs), the main components of atherosclerotic plaque, switch from contractile to synthetic phenotypes during atherogenesis. Ubiquitylation is crucial in regulating VSMC phenotypes in atherosclerosis, and it can be reversely regulated by deubiquitinases. However, the specific effects of deubiquitinases on atherosclerosis have not been thoroughly elucidated. In this study, RNAi screening in human aortic smooth muscle cells was performed to explore the effects of OTU family deubiquitinases, which revealed that silencing OTUB1 inhibited PDGF-BB-stimulated VSMC phenotype switch. Further in vivo studies using Apoe−/− mice revealed that knockdown of OTUB1 in VSMCs alleviated atherosclerosis plaque burden in the advanced stage and led to a stable plaque phenotype. Moreover, VSMC proliferation and migration upon PDGF-BB stimulation could be inhibited by silencing OTUB1 in vitro. Unbiased RNA-sequencing data indicated that knocking down OTUB1 influenced VSMC differentiation, adhesion, and proliferation. Mass spectrometry of ubiquitinated protein confirmed that proteins related to cell growth and migration were differentially ubiquitylated. Mechanistically, we found that OTUB1 recognized the K707 residue ubiquitylation of PDGFRβ with its catalytic triad, thereby reducing the K48-linked ubiquitylation of PDGFRβ. Inhibiting OTUB1 in VSMCs could promote PDGFRβ degradation via the ubiquitin–proteasome pathway, so it was beneficial in preventing VSMCs’ phenotype switch. These findings revealed that knocking down OTUB1 ameliorated VSMCs’ phenotype switch and atherosclerosis progression, indicating that OTUB1 could be a valuable translational therapeutic target in the future.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":"12 1","pages":""},"PeriodicalIF":8.1,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140635535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Pathological progression of osteoarthritis: a perspective on subchondral bone 骨关节炎的病理发展：软骨下骨的视角

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-04-15 DOI: 10.1007/s11684-024-1061-y

Xuefei Li, Wenhua Chen, Dan Liu, Pinghua Chen, Shiyun Wang, Fangfang Li, Qian Chen, Shunyi Lv, Fangyu Li, Chen Chen, Suxia Guo, Weina Yuan, Pan Li, Zhijun Hu

{"title":"Pathological progression of osteoarthritis: a perspective on subchondral bone","authors":"Xuefei Li, Wenhua Chen, Dan Liu, Pinghua Chen, Shiyun Wang, Fangfang Li, Qian Chen, Shunyi Lv, Fangyu Li, Chen Chen, Suxia Guo, Weina Yuan, Pan Li, Zhijun Hu","doi":"10.1007/s11684-024-1061-y","DOIUrl":"https://doi.org/10.1007/s11684-024-1061-y","url":null,"abstract":"Osteoarthritis (OA) is a degenerative bone disease associated with aging. The rising global aging population has led to a surge in OA cases, thereby imposing a significant socioeconomic burden. Researchers have been keenly investigating the mechanisms underlying OA. Previous studies have suggested that the disease starts with synovial inflammation and hyperplasia, advancing toward cartilage degradation. Ultimately, subchondral-bone collapse, sclerosis, and osteophyte formation occur. This progression is deemed as “top to bottom.” However, recent research is challenging this perspective by indicating that initial changes occur in subchondral bone, precipitating cartilage breakdown. In this review, we elucidate the epidemiology of OA and present an in-depth overview of the subchondral bone’s physiological state, functions, and the varied pathological shifts during OA progression. We also introduce the role of multifunctional signal pathways (including osteoprotegerin (OPG)/receptor activator of nuclear factor-kappa B ligand (RANKL)/receptor activator of nuclear factor-kappa B (RANK), and chemokine (CXC motif) ligand 12 (CXCL12)/CXC motif chemokine receptor 4 (CXCR4)) in the pathology of subchondral bone and their role in the “bottom-up” progression of OA. Using vivid pattern maps and clinical images, this review highlights the crucial role of subchondral bone in driving OA progression, illuminating its interplay with the condition.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":"39 1","pages":""},"PeriodicalIF":8.1,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140587323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Cancer stem cell-immune cell crosstalk in the tumor microenvironment for liver cancer progression 肿瘤微环境中癌症干细胞与免疫细胞之间的串扰促进肝癌进展

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-04-11 DOI: 10.1007/s11684-023-1049-z

Yue Ma, Hongwei Lv, Fuxue Xing, Wei Xiang, Zixin Wu, Qiyu Feng, Hongyang Wang, Wen Yang

引用次数: 0

Cross-sectional network analysis of plasma proteins/metabolites correlated with pathogenesis and therapeutic response in acute promyelocytic leukemia. 与急性早幼粒细胞白血病发病机制和治疗反应相关的血浆蛋白/代谢物的横断面网络分析。

IF 8.1 3区医学

Frontiers of Medicine Pub Date : 2024-04-01 Epub Date: 2023-12-27 DOI: 10.1007/s11684-023-1022-x

Niu Qiao, Yizhu Lyu, Feng Liu, Yuliang Zhang, Xiaolin Ma, Xiaojing Lin, Junyu Wang, Yinyin Xie, Ruihong Zhang, Jing Qiao, Hongming Zhu, Li Chen, Hai Fang, Tong Yin, Zhu Chen, Qiang Tian, Saijuan Chen

{"title":"Cross-sectional network analysis of plasma proteins/metabolites correlated with pathogenesis and therapeutic response in acute promyelocytic leukemia.","authors":"Niu Qiao, Yizhu Lyu, Feng Liu, Yuliang Zhang, Xiaolin Ma, Xiaojing Lin, Junyu Wang, Yinyin Xie, Ruihong Zhang, Jing Qiao, Hongming Zhu, Li Chen, Hai Fang, Tong Yin, Zhu Chen, Qiang Tian, Saijuan Chen","doi":"10.1007/s11684-023-1022-x","DOIUrl":"10.1007/s11684-023-1022-x","url":null,"abstract":"The treatment of PML/RARA+ acute promyelocytic leukemia (APL) with all-trans-retinoic acid and arsenic trioxide (ATRA/ATO) has been recognized as a model for translational medicine research. Though an altered microenvironment is a general cancer hallmark, how APL blasts shape their plasma composition is poorly understood. Here, we reported a cross-sectional correlation network to interpret multilayered datasets on clinical parameters, proteomes, and metabolomes of paired plasma samples from patients with APL before or after ATRA/ATO induction therapy. Our study revealed the two prominent features of the APL plasma, suggesting a possible involvement of APL blasts in modulating plasma composition. One was characterized by altered secretory protein and metabolite profiles correlating with heightened proliferation and energy consumption in APL blasts, and the other featured APL plasma-enriched proteins or enzymes catalyzing plasma-altered metabolites that were potential trans-regulatory targets of PML/RARA. Furthermore, results indicated heightened interferon-gamma signaling characterizing a tumor-suppressing function of the immune system at the first hematological complete remission stage, which likely resulted from therapy-induced cell death or senescence and ensuing supraphysiological levels of intracellular proteins. Overall, our work sheds new light on the pathophysiology and treatment of APL and provides an information-rich reference data cohort for the exploratory and translational study of leukemia microenvironment.","PeriodicalId":12558,"journal":{"name":"Frontiers of Medicine","volume":" ","pages":"327-343"},"PeriodicalIF":8.1,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139048621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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