Cell host & microbe最新文献

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Guilds as guides for health vs. disease 公会作为健康与疾病的指南
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.010
Antonio L.C. Gomes, Robert R. Jenq
{"title":"Guilds as guides for health vs. disease","authors":"Antonio L.C. Gomes, Robert R. Jenq","doi":"10.1016/j.chom.2024.11.010","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.010","url":null,"abstract":"In a recent <em>Cell</em> paper, Wu et al. identified microbiome guilds based on bacterial co-occurrence among type 2 diabetes patients. Two competing guilds, associated with high-fiber vs. control diets, correlated with healthy biomarkers. The potential of this approach was further verified across 15 diseases in 26 studies.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"119 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804855","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}
引用次数: 0
HAMpering infection: Helicase ratcheting emerges as a phage-sensing mechanism 阻碍感染:解旋酶棘轮作为噬菌体感应机制出现
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.009
Zhifeng Zeng, Wenyuan Han
{"title":"HAMpering infection: Helicase ratcheting emerges as a phage-sensing mechanism","authors":"Zhifeng Zeng, Wenyuan Han","doi":"10.1016/j.chom.2024.11.009","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.009","url":null,"abstract":"The sensing of pathogens is the first step for any immune response. A recent paper in <em>Cell</em> reveals that the bacterial Hachiman anti-phage defense system deploys a helicase subunit to sense phage invasion via 3′ DNA recognition and subsequent domain rotation to enable nuclease activation.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"111 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804856","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}
引用次数: 0
The bad neighbor: Prophage competition in Salmonella during macrophage infection 坏邻居:巨噬细胞感染时沙门氏菌的前噬菌体竞争
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.11.011
Zoe Netter
{"title":"The bad neighbor: Prophage competition in Salmonella during macrophage infection","authors":"Zoe Netter","doi":"10.1016/j.chom.2024.11.011","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.011","url":null,"abstract":"Sargen and Helaine discover a prophage competition element in <em>Salmonella</em> that inhibits the lytic cycle of co-resident prophages by cleaving a subset of cellular tRNAs. During <em>Salmonella</em> pathogenesis in macrophages, a persister subset experiences prophage induction and competition, reducing release of immunogenic cellular components and altering macrophage response to infection.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"9 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804857","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}
引用次数: 0
Exploring the early life gut microbiome with MAGIC 用MAGIC探索生命早期肠道微生物群
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-11 DOI: 10.1016/j.chom.2024.10.019
Edoardo Pasolli
{"title":"Exploring the early life gut microbiome with MAGIC","authors":"Edoardo Pasolli","doi":"10.1016/j.chom.2024.10.019","DOIUrl":"https://doi.org/10.1016/j.chom.2024.10.019","url":null,"abstract":"In this issue of <em>Cell Host &amp; Microbe</em>, Peng et al. provide the MAGIC catalog as a resource for studying bacterial and viral diversity of the global gut microbiome in early life. By addressing gaps in geographic and age representation, this database enhances our understanding of early microbiome dynamics.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"1 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142804537","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}
引用次数: 0
Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation I型ifn介导的NET释放促进结核分枝杆菌复制并与肉芽肿干酪化有关
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-04 DOI: 10.1016/j.chom.2024.11.008
Chanchal Sur Chowdhury, Rachel L. Kinsella, Michael E. McNehlan, Sumanta K. Naik, Daniel S. Lane, Priyanka Talukdar, Asya Smirnov, Neha Dubey, Ananda N. Rankin, Samuel R. McKee, Reilly Woodson, Abigail Hii, Sthefany M. Chavez, Darren Kreamalmeyer, Wandy Beatty, Joshua T. Mattila, Christina L. Stallings
{"title":"Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma caseation","authors":"Chanchal Sur Chowdhury, Rachel L. Kinsella, Michael E. McNehlan, Sumanta K. Naik, Daniel S. Lane, Priyanka Talukdar, Asya Smirnov, Neha Dubey, Ananda N. Rankin, Samuel R. McKee, Reilly Woodson, Abigail Hii, Sthefany M. Chavez, Darren Kreamalmeyer, Wandy Beatty, Joshua T. Mattila, Christina L. Stallings","doi":"10.1016/j.chom.2024.11.008","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.008","url":null,"abstract":"Neutrophils are the most abundant cell type in the airways of tuberculosis patients. <em>Mycobacterium tuberculosis</em> (<em>Mtb</em>) infection induces the release of neutrophil extracellular traps (NETs); however, the molecular regulation and impact of NET release on <em>Mtb</em> pathogenesis are unknown. We find that during <em>Mtb</em> infection in neutrophils, PAD4 citrullinates histones to decondense chromatin that gets released as NETs in a manner that can maintain neutrophil viability and promote <em>Mtb</em> replication. Type I interferon promotes the formation of chromatin-containing vesicles that allow NET release without compromising plasma membrane integrity. Analysis of nonhuman primate granulomas supports a model where neutrophils are exposed to type I interferon from macrophages as they migrate into the granuloma, thereby enabling the release of NETs associated with necrosis and caseation. Our data reveal NET release as a promising target to inhibit <em>Mtb</em> pathogenesis.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"199 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142763488","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}
引用次数: 0
Cas10 relieves host growth arrest to facilitate spacer retention during type III-A CRISPR-Cas immunity 在III-A型CRISPR-Cas免疫过程中,Cas10缓解宿主生长停滞,促进间隔物保留
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-02 DOI: 10.1016/j.chom.2024.11.005
Naama Aviram, Amanda K. Shilton, Nia G. Lyn, Bernardo S. Reis, Amir Brivanlou, Luciano A. Marraffini
{"title":"Cas10 relieves host growth arrest to facilitate spacer retention during type III-A CRISPR-Cas immunity","authors":"Naama Aviram, Amanda K. Shilton, Nia G. Lyn, Bernardo S. Reis, Amir Brivanlou, Luciano A. Marraffini","doi":"10.1016/j.chom.2024.11.005","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.005","url":null,"abstract":"Cells from all kingdoms of life can enter growth arrest in unfavorable environmental conditions. Key to this process are mechanisms enabling recovery from this state. Staphylococcal type III-A CRISPR-Cas loci encode the Cas10 complex that uses a guide RNA to locate complementary viral transcripts and start an immune response. When the target sequence is expressed late in the viral lytic cycle, defense requires the activity of Csm6, a non-specific RNase that inhibits the growth of the infected cell. How Csm6 protects from infection and whether growth can be restored is not known. Here, we show that growth arrest provides immunity at the population level, preventing viral replication and allowing uninfected cells to propagate. In addition, the ssDNase activity of Cas10 is required for the regrowth of a subset of the arrested cells and the recovery of the infected host, presumably ending the immune response through degradation of the viral DNA.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"12 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142760610","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}
引用次数: 0
Campylobacter jejuni-derived cytolethal distending toxin promotes colorectal cancer metastasis 空肠弯曲杆菌衍生的细胞致死膨胀毒素促进结直肠癌转移
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-12-02 DOI: 10.1016/j.chom.2024.11.006
Zhen He, Jing Yu, Junli Gong, Jinjie Wu, Xuan Zong, Zhanhao Luo, Xiaowen He, Wai Ming Cheng, Yugeng Liu, Chen Liu, Qiang Zhang, Lei Dai, Tao Ding, Beile Gao, Raad Z. Gharaibeh, Jinlin Huang, Christian Jobin, Ping Lan
{"title":"Campylobacter jejuni-derived cytolethal distending toxin promotes colorectal cancer metastasis","authors":"Zhen He, Jing Yu, Junli Gong, Jinjie Wu, Xuan Zong, Zhanhao Luo, Xiaowen He, Wai Ming Cheng, Yugeng Liu, Chen Liu, Qiang Zhang, Lei Dai, Tao Ding, Beile Gao, Raad Z. Gharaibeh, Jinlin Huang, Christian Jobin, Ping Lan","doi":"10.1016/j.chom.2024.11.006","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.006","url":null,"abstract":"Various forms of solid tumors harbor intracellular bacteria, but the physiological consequences of these microorganisms are poorly understood. We show that <em>Campylobacter</em> is significantly enriched in primary colorectal cancer (CRC) lesions from patients with metastasis. <em>Campylobacter</em> <em>jejuni</em>-derived cytolethal distending toxin (CDT) promotes CRC metastasis through JAK2-STAT3-MMP9 signaling in liver or pulmonary metastatic mice models, as confirmed in <em>C. jejuni</em>-infected human colonic tissue and CDT-treated colonic tumoroids from patients. Genetic deletion of <em>cdtB</em> (<em>ΔcdtB</em>) or purified CdtB protein demonstrates that the genotoxin is essential for <em>C. jejuni’s</em> pro-metastatic property. In <em>C.-jejuni</em>-colonized mice, increased translocation of CDT-producing <em>C. jejuni</em> to extraintestinal implanted tumors potentially leads to accelerated metastasis of these tumors. Overall, these findings demonstrate that an intratumor-bacteria-derived genotoxin accelerates tumor metastasis, potentially opening a new diagnostic and therapeutic avenue for cancer management.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"17 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142760389","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}
引用次数: 0
Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19 颅-脑膜-脑轴刺突蛋白的持续存在可能导致COVID-19的神经系统后遗症
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-11-29 DOI: 10.1016/j.chom.2024.11.007
Zhouyi Rong, Hongcheng Mai, Gregor Ebert, Saketh Kapoor, Victor G. Puelles, Jan Czogalla, Senbin Hu, Jinpeng Su, Danilo Prtvar, Inderjeet Singh, Julia Schädler, Claire Delbridge, Hanno Steinke, Hannah Frenzel, Katja Schmidt, Christian Braun, Gina Bruch, Viktoria Ruf, Mayar Ali, Kurt-Wolfram Sühs, Ali Ertürk
{"title":"Persistence of spike protein at the skull-meninges-brain axis may contribute to the neurological sequelae of COVID-19","authors":"Zhouyi Rong, Hongcheng Mai, Gregor Ebert, Saketh Kapoor, Victor G. Puelles, Jan Czogalla, Senbin Hu, Jinpeng Su, Danilo Prtvar, Inderjeet Singh, Julia Schädler, Claire Delbridge, Hanno Steinke, Hannah Frenzel, Katja Schmidt, Christian Braun, Gina Bruch, Viktoria Ruf, Mayar Ali, Kurt-Wolfram Sühs, Ali Ertürk","doi":"10.1016/j.chom.2024.11.007","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.007","url":null,"abstract":"SARS-CoV-2 infection is associated with long-lasting neurological symptoms, although the underlying mechanisms remain unclear. Using optical clearing and imaging, we observed the accumulation of SARS-CoV-2 spike protein in the skull-meninges-brain axis of human COVID-19 patients, persisting long after viral clearance. Further, biomarkers of neurodegeneration were elevated in the cerebrospinal fluid from long COVID patients, and proteomic analysis of human skull, meninges, and brain samples revealed dysregulated inflammatory pathways and neurodegeneration-associated changes. Similar distribution patterns of the spike protein were observed in SARS-CoV-2-infected mice. Injection of spike protein alone was sufficient to induce neuroinflammation, proteome changes in the skull-meninges-brain axis, anxiety-like behavior, and exacerbated outcomes in mouse models of stroke and traumatic brain injury. Vaccination reduced but did not eliminate spike protein accumulation after infection in mice. Our findings suggest persistent spike protein at the brain borders may contribute to lasting neurological sequelae of COVID-19.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"17 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142742584","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}
引用次数: 0
Protection against Clostridioides difficile disease by a naturally avirulent strain 用天然无毒菌株预防艰难梭菌病
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-11-27 DOI: 10.1016/j.chom.2024.11.003
Qiwen Dong, Stephen Harper, Emma McSpadden, Sophie S. Son, Marie-Maude Allen, Huaiying Lin, Rita C. Smith, Carolyn Metcalfe, Victoria Burgo, Che Woodson, Anitha Sundararajan, Amber Rose, Mary McMillin, David Moran, Jessica Little, Michael W. Mullowney, Ashley M. Sidebottom, Louis-Charles Fortier, Aimee Shen, Eric G. Pamer
{"title":"Protection against Clostridioides difficile disease by a naturally avirulent strain","authors":"Qiwen Dong, Stephen Harper, Emma McSpadden, Sophie S. Son, Marie-Maude Allen, Huaiying Lin, Rita C. Smith, Carolyn Metcalfe, Victoria Burgo, Che Woodson, Anitha Sundararajan, Amber Rose, Mary McMillin, David Moran, Jessica Little, Michael W. Mullowney, Ashley M. Sidebottom, Louis-Charles Fortier, Aimee Shen, Eric G. Pamer","doi":"10.1016/j.chom.2024.11.003","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.003","url":null,"abstract":"<em>Clostridioides difficile</em> is a leading cause of healthcare infections. Gut dysbiosis promotes <em>C. difficile</em> infection (CDI) and CDIs promote gut dysbiosis, leading to frequent CDI recurrence. Although therapies preventing recurrent CDI have been developed, including live biotherapeutic products, existing therapies are costly and do not prevent primary infections. Here, we show that an avirulent <em>C. difficile</em> isolate, ST1-75, protects mice from developing colitis induced by a virulent R20291 strain when coinfected at a 1:1 ratio. In metabolic analyses, avirulent ST1-75 depletes amino acids more rapidly than virulent R20291 and supplementation with amino acids ablates this competitive advantage, indicating that ST1-75 limits the growth of virulent R20291 through amino acid depletion. Overall, our study identifies inter-strain nutrient depletion as a potentially exploitable mechanism to reduce the incidence of CDI and reveals that the ST1-75 strain may be a biotherapeutic agent that can prevent CDI in high-risk patients.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"1 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718621","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}
引用次数: 0
Zinc promotes microbial p-coumaric acid production that protects against cholestatic liver injury 锌能促进微生物产生对香豆酸,从而防止胆汁淤积性肝损伤
IF 30.3 1区 医学
Cell host & microbe Pub Date : 2024-11-27 DOI: 10.1016/j.chom.2024.11.002
Dongping Li, Meijuan Wan, Lanfeng Xue, Zhelin Zhang, Yifeng Qiu, Fengyi Mei, Niexing Tang, Chunxiao Yu, Yao Yu, Tianqi Chen, Xing Ding, Qin Yang, Qiuyan Liu, Peng Gu, Wei Jia, Yu Chen, Peng Chen
{"title":"Zinc promotes microbial p-coumaric acid production that protects against cholestatic liver injury","authors":"Dongping Li, Meijuan Wan, Lanfeng Xue, Zhelin Zhang, Yifeng Qiu, Fengyi Mei, Niexing Tang, Chunxiao Yu, Yao Yu, Tianqi Chen, Xing Ding, Qin Yang, Qiuyan Liu, Peng Gu, Wei Jia, Yu Chen, Peng Chen","doi":"10.1016/j.chom.2024.11.002","DOIUrl":"https://doi.org/10.1016/j.chom.2024.11.002","url":null,"abstract":"Cholestatic liver disease (CLD) is a common liver disorder with limited treatment options. Here, we demonstrate that zinc (Zn) supplementation can alter the gut microbiome to mitigate cholestatic liver injury. Oral Zn altered the microbiota of mice and humans (this study was registered at <span><span>clinicaltrials.gov</span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> [NCT05597137]), increasing the abundance of <em>Blautia producta</em> (<em>B. producta</em>) and promoting the generation of p-coumaric acid. Additionally, p-coumaric acid concentrations were negatively correlated with liver injury parameters in CLD patients. In mice, the protective effects of Zn were partially mediated by p-coumaric acid, which directly bound to nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and suppressed the production of reactive oxygen species (ROS) in hepatocytes, thus preventing hepatocyte cell death and liver damage. Additionally, knocking out the histidine ammonia-lyase, which catalyzes the conversion of tyrosine to p-coumaric acid in <em>B. producta</em>, blunted the protective effects of Zn. These findings highlight a host-microbiota interaction that is stimulated by Zn supplementation, providing potential benefits for CLD.","PeriodicalId":9693,"journal":{"name":"Cell host & microbe","volume":"79 1","pages":""},"PeriodicalIF":30.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142718622","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}
引用次数: 0
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