{"title":"Role and mechanism of gut microbiota and metabolites in schizophrenia complicated with sleep disorder","authors":"Ziqi Huang, Zixuan Huang, Zhiqiang Du, Xuezheng Gao, Ying Jiang, Zhenhe Zhou, Haohao Zhu","doi":"10.1080/19490976.2025.2607817","DOIUrl":"https://doi.org/10.1080/19490976.2025.2607817","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"2 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-29DOI: 10.1080/19490976.2025.2604908
Ananya Parthasarathy, Tingting Li, Karen L. Edelblum
{"title":"Crosstalk between the microbiota and intestinal γδ T cell compartments in health and IBD","authors":"Ananya Parthasarathy, Tingting Li, Karen L. Edelblum","doi":"10.1080/19490976.2025.2604908","DOIUrl":"https://doi.org/10.1080/19490976.2025.2604908","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"29 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145847402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-27DOI: 10.1080/19490976.2025.2607076
Marwh G. Aldriwesh, Raniah S. Alotibi, Nasser Alqurainy, Shatha Alrabiah, Assad M. Arafah, Majed F. Alghoribi, Reham Ajina
{"title":"The role of gut microbiome in aging-associated diseases: where do we stand now and how technology will transform the future","authors":"Marwh G. Aldriwesh, Raniah S. Alotibi, Nasser Alqurainy, Shatha Alrabiah, Assad M. Arafah, Majed F. Alghoribi, Reham Ajina","doi":"10.1080/19490976.2025.2607076","DOIUrl":"https://doi.org/10.1080/19490976.2025.2607076","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"22 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2025-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145836126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-27DOI: 10.1080/19490976.2025.2604868
Efrain Ricardo Torres, Jennifer Wilcox, W. H. Wilson Tang
{"title":"Gut‒heart axis: emerging therapies targeting trimethylamine N-oxide production","authors":"Efrain Ricardo Torres, Jennifer Wilcox, W. H. Wilson Tang","doi":"10.1080/19490976.2025.2604868","DOIUrl":"https://doi.org/10.1080/19490976.2025.2604868","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"27 1","pages":""},"PeriodicalIF":12.2,"publicationDate":"2025-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145836130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Enterohemorrhagic Escherichia coli (EHEC) is a leading foodborne pathogen worldwide that causes severe diarrheal disease, hemorrhagic colitis, and hemolytic uremic syndrome, representing a significant threat to public health. O-islands are discrete genomic regions absent from nonpathogenic E. coli K-12 but present in EHEC O157:H7, many of which correspond to or overlap with pathogenicity islands (PAIs) that contribute to virulence. Among these O-islands, O‑Island 28 (OI‑28) in EHEC O157:H7 is a conserved genomic island predicted to encode a complete type I secretion system (T1SS) and two RTX family proteins, but its role in pathogenesis has remained unclear. Here, we show that deletion of OI‑28 markedly reduces epithelial adherence and intestinal colonization in mice without affecting in vitro growth. Mechanistically, OI‑28 is activated by the response regulator RstA, and RstA binds directly to the OI‑28 regulatory region. Consistent with the calcium-dependent folding of RTX adhesins, extracellular Ca2+ enhances OI‑28 expression and T1SS-dependent adherence in an RstA-dependent manner, and dietary calcium depletion reduces early colonization in vivo. Comparative genomics further demonstrated that OI‑28 is required for the colonization of multiple pathogenic E. coli strains. Collectively, these findings demonstrate that OI‑28 is an RstA‑activated, calcium‑responsive T1SS secretion system that is conserved across pathogenic E. coli strains and is essential for efficient epithelial adherence and early intestinal colonization.
{"title":"O‑Island 28 encodes a type I secretion and RTX adhesion system regulated by RstA and required for early EHEC O157:H7 adherence.","authors":"Tianshui Niu,Mengqian Huang,Fei He,Xianjuan Yu,Aifeng Chen,Yan Shi,Jiaying Han,Xiang Lian,Junwei Su,Yutao Liu,Chuhui Ru","doi":"10.1080/19490976.2025.2609461","DOIUrl":"https://doi.org/10.1080/19490976.2025.2609461","url":null,"abstract":"Enterohemorrhagic Escherichia coli (EHEC) is a leading foodborne pathogen worldwide that causes severe diarrheal disease, hemorrhagic colitis, and hemolytic uremic syndrome, representing a significant threat to public health. O-islands are discrete genomic regions absent from nonpathogenic E. coli K-12 but present in EHEC O157:H7, many of which correspond to or overlap with pathogenicity islands (PAIs) that contribute to virulence. Among these O-islands, O‑Island 28 (OI‑28) in EHEC O157:H7 is a conserved genomic island predicted to encode a complete type I secretion system (T1SS) and two RTX family proteins, but its role in pathogenesis has remained unclear. Here, we show that deletion of OI‑28 markedly reduces epithelial adherence and intestinal colonization in mice without affecting in vitro growth. Mechanistically, OI‑28 is activated by the response regulator RstA, and RstA binds directly to the OI‑28 regulatory region. Consistent with the calcium-dependent folding of RTX adhesins, extracellular Ca2+ enhances OI‑28 expression and T1SS-dependent adherence in an RstA-dependent manner, and dietary calcium depletion reduces early colonization in vivo. Comparative genomics further demonstrated that OI‑28 is required for the colonization of multiple pathogenic E. coli strains. Collectively, these findings demonstrate that OI‑28 is an RstA‑activated, calcium‑responsive T1SS secretion system that is conserved across pathogenic E. coli strains and is essential for efficient epithelial adherence and early intestinal colonization.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"5 1","pages":"2609461"},"PeriodicalIF":12.2,"publicationDate":"2025-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145844798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-24DOI: 10.1080/19490976.2025.2604334
Yuan Li,Caiming Xu,Hyun Park,Ashten N Omstead,Muhammad Anees,Chris Sherry,Alisha F Khan,Erin Grayhack,Benny Weksler,Patrick Wagner,David L Bartlett,Stephen J Meltzer,Ali H Zaidi,Ajay Goel
Esophageal adenocarcinoma (EAC) has seen a dramatic rise in incidence in developed countries over the past three decades. Early detection of its precursors-gastroesophageal reflux disease (GERD), Barrett's esophagus (BE), and high-grade dysplasia (HGD) is critical for cancer prevention. This study presents the development and validation of a novel liquid biopsy assay based on circulating microbial DNA (cmDNA) for the early detection of EAC and HGD. Using metagenomic sequencing, we identified significant differences in microbial diversity and composition between EAC and HGD patients, as well as between BE and GERD patients. A total of 46 microbial candidates in tissue and 419 in serum were upregulated in EAC & HGD, with 11 consistently elevated in both sample types. Following qRT-PCR validation and LASSO regression, a 6-marker cmDNA panel was selected. This signature was incorporated into a diagnostic model trained with the XGBoost algorithm, achieving an AUC of 0.93 in the training cohort (52 HGD & EAC cases vs. 54 BE & GERD controls). Importantly, the model demonstrated robust performance in an independent testing cohort (23 HGD & EAC cases vs. 22 BE & GERD controls), yielding AUCs of 0.91 for EAC and 0.88 for HGD. These findings highlight the diagnostic potential of cmDNA-based profiling and support its utility as a minimally invasive, accurate, and generalizable tool for early detection of esophageal adenocarcinoma.
{"title":"A machine-learning informed circulating microbial DNA signature for early diagnosis of esophageal adenocarcinoma.","authors":"Yuan Li,Caiming Xu,Hyun Park,Ashten N Omstead,Muhammad Anees,Chris Sherry,Alisha F Khan,Erin Grayhack,Benny Weksler,Patrick Wagner,David L Bartlett,Stephen J Meltzer,Ali H Zaidi,Ajay Goel","doi":"10.1080/19490976.2025.2604334","DOIUrl":"https://doi.org/10.1080/19490976.2025.2604334","url":null,"abstract":"Esophageal adenocarcinoma (EAC) has seen a dramatic rise in incidence in developed countries over the past three decades. Early detection of its precursors-gastroesophageal reflux disease (GERD), Barrett's esophagus (BE), and high-grade dysplasia (HGD) is critical for cancer prevention. This study presents the development and validation of a novel liquid biopsy assay based on circulating microbial DNA (cmDNA) for the early detection of EAC and HGD. Using metagenomic sequencing, we identified significant differences in microbial diversity and composition between EAC and HGD patients, as well as between BE and GERD patients. A total of 46 microbial candidates in tissue and 419 in serum were upregulated in EAC & HGD, with 11 consistently elevated in both sample types. Following qRT-PCR validation and LASSO regression, a 6-marker cmDNA panel was selected. This signature was incorporated into a diagnostic model trained with the XGBoost algorithm, achieving an AUC of 0.93 in the training cohort (52 HGD & EAC cases vs. 54 BE & GERD controls). Importantly, the model demonstrated robust performance in an independent testing cohort (23 HGD & EAC cases vs. 22 BE & GERD controls), yielding AUCs of 0.91 for EAC and 0.88 for HGD. These findings highlight the diagnostic potential of cmDNA-based profiling and support its utility as a minimally invasive, accurate, and generalizable tool for early detection of esophageal adenocarcinoma.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"45 1","pages":"2604334"},"PeriodicalIF":12.2,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145813472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-24DOI: 10.1080/19490976.2025.2601430
Lena K Siewert,Kristina Berve,Elisabeth Pössnecker,Julia Dyckow,Amel Zulji,Ryan Baumann,Aida Munoz-Blazquez,Gurumoorthy Krishnamoorthy,David Schreiner,Sharon Sagan,Charlotte Nelson,Joseph J Sabatino,Kazuki Nagashima,Médéric Diard,Andrew J Macpherson,Stephanie C Ganal-Vonarburg,Michael A Fischbach,Scott S Zamvil,Lucas Schirmer,Sergio E Baranzini,Anne-Katrin Pröbstel
Microbiome-based therapies are promising new treatment avenues. While global alterations in microbiota composition have been shown in multiple sclerosis, whether and how gut microbiota influence autoimmune responses in an antigen-specific manner is unclear. Here, we genetically engineered gut bacteria to express a brain antigen and dissect their pathogenic potential in a murine model of autoimmune neuroinflammation. Colonization with bacteria expressing myelin - but not ovalbumin-peptide exacerbates an encephalitogenic immune response in the gut by activating antigen-specific T cells as well as B cells leading to accelerated neuroinflammatory disease. These results demonstrate how antigen-specific microbial modulation can influence autoimmunity, providing insight for development of therapeutic strategies targeting specific bacterial taxa for treatment of MS and other autoimmune diseases.
{"title":"Antigen-specific activation of gut immune cells drives autoimmune neuroinflammation.","authors":"Lena K Siewert,Kristina Berve,Elisabeth Pössnecker,Julia Dyckow,Amel Zulji,Ryan Baumann,Aida Munoz-Blazquez,Gurumoorthy Krishnamoorthy,David Schreiner,Sharon Sagan,Charlotte Nelson,Joseph J Sabatino,Kazuki Nagashima,Médéric Diard,Andrew J Macpherson,Stephanie C Ganal-Vonarburg,Michael A Fischbach,Scott S Zamvil,Lucas Schirmer,Sergio E Baranzini,Anne-Katrin Pröbstel","doi":"10.1080/19490976.2025.2601430","DOIUrl":"https://doi.org/10.1080/19490976.2025.2601430","url":null,"abstract":"Microbiome-based therapies are promising new treatment avenues. While global alterations in microbiota composition have been shown in multiple sclerosis, whether and how gut microbiota influence autoimmune responses in an antigen-specific manner is unclear. Here, we genetically engineered gut bacteria to express a brain antigen and dissect their pathogenic potential in a murine model of autoimmune neuroinflammation. Colonization with bacteria expressing myelin - but not ovalbumin-peptide exacerbates an encephalitogenic immune response in the gut by activating antigen-specific T cells as well as B cells leading to accelerated neuroinflammatory disease. These results demonstrate how antigen-specific microbial modulation can influence autoimmunity, providing insight for development of therapeutic strategies targeting specific bacterial taxa for treatment of MS and other autoimmune diseases.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"1 1","pages":"2601430"},"PeriodicalIF":12.2,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145813473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gut microbiota dysbiosis contributes to acute pancreatitis (AP) severity, but the specific microbes and mechanisms remain unclear. In this study, we employed both germ-free (GF) and specific-pathogen-free (SPF) murine models of AP to investigate the role of the intestinal microbiota. Our findings demonstrate that GF mice exhibited markedly attenuated pancreatic injury, inflammatory cell infiltration, and neutrophil extracellular traps (NETs) formation. Through fecal microbiota transplantation (FMT) from AP patients, differential antibiotic modulation, and single-bacterial colonization experiments, we identified Gram-negative bacteria, particularly Escherichia coli (E. coli), as critical microbial drivers of disease exacerbation. Single-cell RNA sequencing revealed that microbiota dysbiosis profoundly reprogrammed both local pancreatic and systemic immune landscapes. Specifically, dysbiosis promoted emergency granulopoiesis in the bone marrow, enhanced neutrophil mobilization and activation, and facilitated the expansion of pro-inflammatory neutrophil subpopulations (Neutrophils_2 and Neutrophils_3). These subsets exhibited upregulated signaling through NETosis-associated pathways, including TLR, NF-κB, and IL-17 axes. Conversely, in GF conditions, we observed a predominance of an anti-inflammatory neutrophil subset (Neutrophils_4), characterized by the expression of tissue repair-associated genes such as Reg1 and Reg2. Shotgun metagenomic profiling of fecal samples from patients with AP revealed an enrichment of E. coli during the acute phase, positively correlating with circulating cell-free DNA, a marker of NETosis. Together, these insights suggest that gut microbiota dysbiosis, notably increased E. coli abundance, may aggravate AP by reshaping immunity and promoting aberrant NETs formation, supporting microbiota or NETs targeted therapies.
{"title":"Gut microbiota dysbiosis exacerbates acute pancreatitis via Escherichia coli-driven neutrophil heterogeneity and NETosis.","authors":"Yaoyu Zou,Nianshuang Li,Xueyang Li,Maobin Kuang,Xin Xu,Langyi Guan,Xin Li,Pan Zheng,Leyan Li,Jianhua Wan,Nonghua Lu,Jianping Liu,Cong He,Yin Zhu","doi":"10.1080/19490976.2025.2606480","DOIUrl":"https://doi.org/10.1080/19490976.2025.2606480","url":null,"abstract":"Gut microbiota dysbiosis contributes to acute pancreatitis (AP) severity, but the specific microbes and mechanisms remain unclear. In this study, we employed both germ-free (GF) and specific-pathogen-free (SPF) murine models of AP to investigate the role of the intestinal microbiota. Our findings demonstrate that GF mice exhibited markedly attenuated pancreatic injury, inflammatory cell infiltration, and neutrophil extracellular traps (NETs) formation. Through fecal microbiota transplantation (FMT) from AP patients, differential antibiotic modulation, and single-bacterial colonization experiments, we identified Gram-negative bacteria, particularly Escherichia coli (E. coli), as critical microbial drivers of disease exacerbation. Single-cell RNA sequencing revealed that microbiota dysbiosis profoundly reprogrammed both local pancreatic and systemic immune landscapes. Specifically, dysbiosis promoted emergency granulopoiesis in the bone marrow, enhanced neutrophil mobilization and activation, and facilitated the expansion of pro-inflammatory neutrophil subpopulations (Neutrophils_2 and Neutrophils_3). These subsets exhibited upregulated signaling through NETosis-associated pathways, including TLR, NF-κB, and IL-17 axes. Conversely, in GF conditions, we observed a predominance of an anti-inflammatory neutrophil subset (Neutrophils_4), characterized by the expression of tissue repair-associated genes such as Reg1 and Reg2. Shotgun metagenomic profiling of fecal samples from patients with AP revealed an enrichment of E. coli during the acute phase, positively correlating with circulating cell-free DNA, a marker of NETosis. Together, these insights suggest that gut microbiota dysbiosis, notably increased E. coli abundance, may aggravate AP by reshaping immunity and promoting aberrant NETs formation, supporting microbiota or NETs targeted therapies.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"45 1","pages":"2606480"},"PeriodicalIF":12.2,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145813470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-23DOI: 10.1080/19490976.2025.2604871
Jarrah M Dowrick,Nicole C Roy,Caterina Carco,Shanalee C James,Phoebe E Heenan,Chris M A Frampton,Karl Fraser,Wayne Young,Janine Cooney,Tania Trower,Jacqueline I Keenan,Warren C McNabb,Jane A Mullaney,Simone B Bayer,Nicholas J Talley,Richard B Gearry,Timothy R Angeli-Gordon
Rome IV disorders of gut-brain interaction (DGBI) subtypes are known to be unstable and demonstrate high rates of non-treatment response, likely indicating patient heterogeneity. Cluster analysis, a type of unsupervised machine learning, can identify homogeneous sub-populations. Independent cluster analyses of symptom and biological data have highlighted its value in predicting patient outcomes. Integrated clustering of symptom and biological data may provide a unique multimodal perspective that better captures the complexity of DGBI. Here, integrated symptom and multi-omic cluster analysis was performed on a cohort of healthy controls and patients with lower-gastrointestinal tract DGBI. Cluster stability was assessed by considering how frequently pairs of participants appeared in the same cluster between different bootstrapped datasets. Functional enrichment analysis was performed on the biological signatures of stable DGBI-predominant clusters, implicating disrupted ammonia handling and metabolism as possible pathophysiologies present in a subset of patients with DGBI. Integrated clustering revealed subtypes that were not apparent using a singular modality, suggesting a symptom-only classification is prone to capturing heterogeneous sub-populations.
{"title":"Integrated multi-omic and symptom clustering reveals lower-gastrointestinal disorders of gut-brain interaction heterogeneity.","authors":"Jarrah M Dowrick,Nicole C Roy,Caterina Carco,Shanalee C James,Phoebe E Heenan,Chris M A Frampton,Karl Fraser,Wayne Young,Janine Cooney,Tania Trower,Jacqueline I Keenan,Warren C McNabb,Jane A Mullaney,Simone B Bayer,Nicholas J Talley,Richard B Gearry,Timothy R Angeli-Gordon","doi":"10.1080/19490976.2025.2604871","DOIUrl":"https://doi.org/10.1080/19490976.2025.2604871","url":null,"abstract":"Rome IV disorders of gut-brain interaction (DGBI) subtypes are known to be unstable and demonstrate high rates of non-treatment response, likely indicating patient heterogeneity. Cluster analysis, a type of unsupervised machine learning, can identify homogeneous sub-populations. Independent cluster analyses of symptom and biological data have highlighted its value in predicting patient outcomes. Integrated clustering of symptom and biological data may provide a unique multimodal perspective that better captures the complexity of DGBI. Here, integrated symptom and multi-omic cluster analysis was performed on a cohort of healthy controls and patients with lower-gastrointestinal tract DGBI. Cluster stability was assessed by considering how frequently pairs of participants appeared in the same cluster between different bootstrapped datasets. Functional enrichment analysis was performed on the biological signatures of stable DGBI-predominant clusters, implicating disrupted ammonia handling and metabolism as possible pathophysiologies present in a subset of patients with DGBI. Integrated clustering revealed subtypes that were not apparent using a singular modality, suggesting a symptom-only classification is prone to capturing heterogeneous sub-populations.","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"37 1","pages":"2604871"},"PeriodicalIF":12.2,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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