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A VLPs based vaccine protects against Zika virus infection and prevents cerebral and testicular damage

NPJ vaccines 2025年第1期10卷 107页

作者： Nelson Côrtes Aline Lira Jaqueline D Q Silva Evelyn Carvalho Wasim A Prates-Syed Barbara Hamaguchi Ricardo Durães-Carvalho Andrea Balan Niels O S Câmara Otavio Cabral-Marques Norbert Pardi Ester C Sabino José E Krieger Gustavo Cabral-Miranda Department of Infectious Diseases and Tropical Medicine Laboratory of Medical Investigation 46 Faculty of Medicine University of São Paulo São Paulo Brazil. Department of Immunology Institute of Biomedical Sciences University of São Paulo São Paulo Brazil. Department of Clinical and Toxicological Analyses School of Pharmaceutical Sciences University of Sao Paulo São Paulo Brazil. Department of Biophysics São Paulo School of Medicine Federal University of São Paulo São Paulo SP Brazil. Department of Microbiology Immunology and Parasitology São Paulo School of Medicine Federal University of São Paulo (UNIFESP) São Paulo SP Brazil. Department of Morphology and Genetics Federal University of São Paulo São Paulo Brazil. Interunit Bioinformatics Graduate Program Institute of Chemistry University of Sao Paulo Sao Paulo Brazil. Applied Structural Biology Laboratory Institute of Biomedical Sciences University of São Paulo São Paulo Brazil. Department of Medicine Division of Molecular Medicine Laboratory of Medical Investigation 29 Faculty of Medicine University of São Paulo São Paulo Brazil. DO'R Institute for Research São Paulo Brazil. Department of Microbiology Perelman School of Medicine University of Pennsylvania Philadelphia PA USA. Department of Pathology Laboratory of Medical Investigation 46 Faculty of Medicine University of São Paulo São Paulo Brazil. Laboratory of Genetics and Molecular Cardiology Clinical Hospital Faculty of Medicine University of São Paulo Heart Institute São Paulo Brazil. Department of Infectious Diseases and Tropical Medicine Laboratory of Medical Investigation 46 Faculty of Medicine University of São Paulo São Paulo Brazil. gcabral.miranda@usp.br. Department of Immunology Institute of Biomedical Sciences University of São Paulo São Paulo Brazil. gcabral.miranda@usp.br.

Still, Zika virus (ZIKV) infection poses a substantial public health risk, especially for pregnant women and their fetuses, as it can result in congenital abnormalities and fetal mortality during pregnancy. Despite significant advances in understanding and combating ZIKV, considerable challenges remain in the fight against this flavivirus. A crucial component of this effort is the development of vaccines, none of which have yet been licensed for human use. Here, we present a comprehensive study of a novel ZIKV vaccine candidate based on virus-like particles (VLPs), designed to provide broad immunological protection against viral infection combined with safety, without the need for additional adjuvants. A self-adjuvanted VLPs-based vaccine displaying the envelope protein domain III (EDIII) of ZIKV was built. The EDIII protein was expressed in E. coli and chemically conjugated to QβVLPs. Immunization of C57BL/6 mice with two doses of the EDIII-QβVLPs vaccine elicited strong EDIII-specific Th1-based immune response. Notably, the vaccine induced neutralizing antibodies and conferred protection in type I IFN receptor-deficient (G129) mice against ZIKV challenge. Furthermore, vaccinated male mice were protected from ZIKV-induced cerebral and testicular damage, critical concerns for ZIKV pathogenesis. These findings suggest that the EDIII-QβVLP vaccine is a promising candidate for preventing ZIKV infection, with potential applications in combatting this and other emerging flaviviruses.

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Correction to: Authors’ Reply to Letter to the Editor: Continued improvement to genetic diversity indicator for CBD

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Conservation Genetics 2021年第4期22卷 537-539页

作者： Laikre, Linda Hohenlohe, Paul A. Allendorf, Fred W. Bertola, Laura D. Breed, Martin F. Bruford, Michael W. Funk, W. Chris Gajardo, Gonzalo González-Rodríguez, Antonio Grueber, Catherine E. Hedrick, Philip W. Heuertz, Myriam Hunter, Margaret E. Johannesson, Kerstin Liggins, Libby MacDonald, Anna J. Mergeay, Joachim Moharrek, Farideh O’Brien, David Ogden, Rob Orozco-terWengel, Pablo Palma-Silva, Clarisse Pierson, Jennifer Paz-Vinas, Ivan Russo, Isa-Rita M. Ryman, Nils Segelbacher, Gernot Sjögren-Gulve, Per Waits, Lisette P. Vernesi, Cristiano Hoban, Sean Division of Population Genetics Department of Zoology Stockholm University Stockholm Sweden Institute for Bioinformatics and Evolutionary Studies Department of Biological Sciences University of Idaho Moscow USA Division of Biological Sciences University of Montana Missoula USA City College of New York New York USA College of Science and Engineering Flinders University Bedford Park Australia School of Biosciences Cardiff University Cardiff Wales UK Graduate Degree Program in Ecology Department of Biology Colorado State University Fort Collins USA Universidad de Los Lagos Lab Genetics Aquaculture & Biodiversity Osorno Chile Instituto de Investigaciones en Ecosistemas y Sustentabilidad Universidad Nacional Autónoma de México Morelia Mexico School of Life and Environmental Sciences Faculty of Science The University of Sydney Sydney Australia School of Life Sciences Arizona State University Tempe USA INRAE Univ. Bordeaux Biogeco Cestas France U.S. Geological Survey Wetland and Aquatic Research Center Gainesville USA Department of Marine Sciences University of Gothenburg Tjärnö Strömstad Sweden School of Natural and Computational Sciences Massey University Auckland New Zealand The John Curtin School of Medical Research/Research School of Biology The Australian National University Acton Australia Research Institute for Nature and Forest Geraardsbergen Belgium Aquatic Ecology Evolution and Conservation KULeuven Leuven Belgium Novo Nordisk Foundation Center for Basic Metabolic Research Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark Faculty of Biological Sciences Tarbiat Modares University Tehran Iran Scottish Natural Heritage Inverness UK Royal (Dick) School of Veterinary Studies and the Roslin Institute University of Edinburgh Midlothian UK Department of Plant Science Institute of Biology University of Campinas Campinas Brazil Australian Wildlife Conservancy Subiaco East Australia Laboratoire Evolution & Div

A correction to this paper has been published: https://***/10.1007/s10592-021-01376-9

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Polygenic risk modeling for prediction of epithelial ovarian cancer risk (vol 30, pg 349, 2021)

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EUROPEAN JOURNAL OF HUMAN GENETICS 2022年第5期30卷 630-631页

作者： Dareng, Eileen O. Tyrer, Jonathan P. Barnes, Daniel R. Jones, Michelle R. Yang, Xin Aben, Katja K. H. Adank, Muriel A. Agata, Simona Andrulis, Irene L. Anton-Culver, Hoda Antonenkova, Natalia N. Aravantinos, Gerasimos Arun, Banu K. Augustinsson, Annelie Balmana, Judith Bandera, Elisa V. Barkardottir, Rosa B. Barrowdale, Daniel Beckmann, Matthias W. Beeghly-Fadiel, Alicia Benitez, Javier Bermisheva, Marina Bernardini, Marcus Q. Bjorge, Line Black, Amanda Bogdanova, Natalia V. Bonanni, Bernardo Borg, Ake Brenton, James D. Budzilowska, Agnieszka Butzow, Ralf Buys, Saundra S. Cai, Hui Caligo, Maria A. Campbell, Ian Cannioto, Rikki Cassingham, Hayley Chang-Claude, Jenny Chanock, Stephen J. Chen, Kexin Chiew, Yoke-Eng Chung, Wendy K. Claes, Kathleen B. M. Colonna, Sarah Cook, Linda S. Couch, Fergus J. Daly, Mary B. Dao, Fanny Davies, Eleanor de la Hoya, Miguel de Putter, Robin Dennis, Joe DePersia, Allison Devilee, Peter Diez, Orland Ding, Yuan Chun Doherty, Jennifer A. Domchek, Susan M. Dork, Thilo du Bois, Andreas Durst, Matthias Eccles, Diana M. Eliassen, Heather A. Engel, Christoph Evans, Gareth D. Fasching, Peter A. Flanagan, James M. Fortner, Renee T. Machackova, Eva Friedman, Eitan Ganz, Patricia A. Garber, Judy Gensini, Francesca Giles, Graham G. Glendon, Gord Godwin, Andrew K. Goodman, Marc T. Greene, Mark H. Gronwald, Jacek Hahnen, Eric Haiman, Christopher A. Hakansson, Niclas Hamann, Ute Hansen, Thomas V. O. Harris, Holly R. Hartman, Mikael Heitz, Florian Hildebrandt, Michelle A. T. Hogdall, Estrid Hogdall, Claus K. Hopper, John L. Huang, Ruea-Yea Huff, Chad Hulick, Peter J. Huntsman, David G. Imyanitov, Evgeny N. Isaacs, Claudine Jakubowska, Anna James, Paul A. Janavicius, Ramunas Jensen, Allan Johannsson, Oskar Th. John, Esther M. Jones, Michael E. Kang, Daehee Karlan, Beth Y. Karnezis, Anthony Kelemen, Linda E. Khusnutdinova, Elza Kiemeney, Lambertus A. Kim, Byoung-Gie Kjaer, Susanne K. Komenaka, Ian Kupryjanczyk, Jolanta Kurian, Allison W. Kwong, Ava Lambrechts, Diether Larson, Melissa C. Lazaro, Conxi L University of Cambridge Centre for Cancer Genetic Epidemiology Department of Public Health and Primary Care Cambridge UK University of Cambridge Centre for Cancer Genetic Epidemiology Department of Oncology Cambridge UK Center for Bioinformatics and Functional Genomics Cedars-Sinai Medical Center Los Angeles CA USA Radboud University Medical Center Radboud Institute for Health Sciences Nijmegen The Netherlands Netherlands Comprehensive Cancer Organisation Utrecht The Netherlands The Netherlands Cancer Institute—Antoni van Leeuwenhoek hospital Family Cancer Clinic Amsterdam The Netherlands Veneto Institute of Oncology IOV—IRCCS Immunology and Molecular Oncology Unit Padua Italy Lunenfeld-Tanenbaum Research Institute of Mount Sinai Hospital Fred A. Litwin Center for Cancer Genetics Toronto ON Canada University of Toronto Department of Molecular Genetics Toronto ON Canada University of California Irvine Department of Epidemiology Genetic Epidemiology Research Institute Irvine CA USA N.N. Alexandrov Research Institute of Oncology and Medical Radiology Minsk Belarus ‘Agii Anargiri’ Cancer Hospital Athens Greece University of Texas MD Anderson Cancer Center Department of Breast Medical Oncology Houston TX USA Lund University Department of Cancer Epidemiology Clinical Sciences Lund Sweden Vall d’Hebron Institute of Oncology Hereditary cancer Genetics Group Barcelona Spain University Hospital of Vall d’Hebron Department of Medical Oncology Barcelona Spain Rutgers Cancer Institute of New Jersey Cancer Prevention and Control Program New Brunswick NJ USA Landspitali University Hospital Department of Pathology Reykjavik Iceland University of Iceland BMC (Biomedical Centre) Faculty of Medicine Reykjavik Iceland University Hospital Erlangen Friedrich-Alexander-University Erlangen-Nuremberg Department of Gynecology and Obstetrics Comprehensive Cancer Center ER-EMN Erlangen Germany Vanderbilt University School of Medicine Division of Epidemiology Department

Polygenic risk scores (PRS) for epithelial ovarian cancer (EOC) have the potential to improve risk stratification. Joint estimation of Single Nucleotide Polymorphism (SNP) effects in models could improve predictive performance over standard approaches of PRS construction. Here, we implemented computationally efficient, penalized, logistic regression models (lasso, elastic net, stepwise) to individual level genotype data and a Bayesian framework with continuous shrinkage, “select and shrink for summary statistics” (S4), to summary level data for epithelial non-mucinous ovarian cancer risk prediction. We developed the models in a dataset consisting of 23,564 non-mucinous EOC cases and 40,138 controls participating in the Ovarian Cancer Association Consortium (OCAC) and validated the best models in three populations of different ancestries: prospective data from 198,101 women of European ancestries; 7,669 women of East Asian ancestries; 1,072 women of African ancestries, and in 18,915 BRCA1 and 12,337 BRCA2 pathogenic variant carriers of European ancestries. In the external validation data, the model with the strongest association for non-mucinous EOC risk derived from the OCAC model development data was the S4 model (27,240 SNPs) with odds ratios (OR) of 1.38 (95% CI: 1.28–1.48, AUC: 0.588) per unit standard deviation, in women of European ancestries; 1.14 (95% CI: 1.08–1.19, AUC: 0.538) in women of East Asian ancestries; 1.38 (95% CI: 1.21–1.58, AUC: 0.593) in women of African ancestries; hazard ratios of 1.36 (95% CI: 1.29–1.43, AUC: 0.592) in BRCA1 pathogenic variant carriers and 1.49 (95% CI: 1.35–1.64, AUC: 0.624) in BRCA2 pathogenic variant carriers. Incorporation of the S4 PRS in risk prediction models for ovarian cancer may have clinical utility in ovarian cancer prevention programs.

关键词： Clinical genetics Genetic markers Risk factors Biomedicine general Human Genetics bioinformatics Gene Expression Cytogenetics

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Void distributions reveal structural link between jammed packings and protein cores

arXiv

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arXiv 2018年

作者： Treado, John D. Mei, Zhe Regan, Lynne O'Hern, Corey S. Department of Mechanical Engineering & Materials Science Yale University New HavenCT06520 United States Integrated Graduate Program in Physical & Engineering Biology Yale University New HavenCT06520 United States Department of Chemistry Yale University New HavenCT06520 United States Department of Molecular Biophysics & Biochemistry Yale University New HavenCT06520 United States Department of Physics Yale University New HavenCT06520 United States Department of Applied Physics Yale University New HavenCT06520 United States Program in Computational Biology and Bioinformatics Yale University New HavenCT06520 United States

Dense packing of hydrophobic residues in the cores of globular proteins determines their stability. Recently, we have shown that protein cores possess packing fraction φ ≈ 0.56, which is the same as dense, random packing of amino acid-shaped particles. In this article, we compare the structural properties of protein cores and jammed packings of amino acid-shaped particles in much greater depth by measuring their local and connected void regions. We find that the distributions of surface Voronoi cell volumes and local porosities obey similar statistics in both systems. We also measure the probability that accessible, connected void regions percolate as a function of the size of a spherical probe particle and show that both systems possess the same critical probe size. By measuring the critical exponent τ that characterizes the size distribution of connected void clusters at the onset of percolation, we show that void percolation in packings of amino acid-shaped particles and protein cores belong to the same universality class, which is different from that for void percolation in jammed sphere packings. We propose that the connected void regions of proteins are a defining feature of proteins and can be used to differentiate experimentally observed proteins from decoy structures that are generated using computational protein design software. This work emphasizes that jammed packings of amino acid-shaped particles can serve as structural and mechanical analogs of protein cores, and could therefore be useful in modeling the response of protein cores to cavity-expanding and -reducing mutations. Copyright © 2018, The Authors. All rights reserved.

关键词： Amino acids

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Author Correction: Effect of de novo transcriptome assembly on transcript quantification

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Scientific reports 2019年第1期9卷 18041页

作者： Ping-Han Hsieh Yen-Jen Oyang Chien-Yu Chen Graduate Institute of Biomedical Electronics and Bioinformatics National Taiwan University Taipei 10617 Taiwan. Department of Computer Science and Information Engineering National Taiwan University Taipei 10617 Taiwan. Department of Bio-Industrial Mechatronics Engineering National Taiwan University Taipei 10617 Taiwan. chienyuchen@ntu.edu.tw. Genome and Systems Biology Program National Taiwan University and Academia sinica Taipei 10617 Taiwan. chienyuchen@ntu.edu.tw.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

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Genetic drivers of heterogeneity in type 2 diabetes pathophysiology

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Nature 2024年第8003期627卷 347-357页

作者： Ken Suzuki Konstantinos Hatzikotoulas Lorraine Southam Henry J Taylor Xianyong Yin Kim M Lorenz Ravi Mandla Alicia Huerta-Chagoya Giorgio E M Melloni Stavroula Kanoni Nigel W Rayner Ozvan Bocher Ana Luiza Arruda Kyuto Sonehara Shinichi Namba Simon S K Lee Michael H Preuss Lauren E Petty Philip Schroeder Brett Vanderwerff Mart Kals Fiona Bragg Kuang Lin Xiuqing Guo Weihua Zhang Jie Yao Young Jin Kim Mariaelisa Graff Fumihiko Takeuchi Jana Nano Amel Lamri Masahiro Nakatochi Sanghoon Moon Robert A Scott James P Cook Jung-Jin Lee Ian Pan Daniel Taliun Esteban J Parra Jin-Fang Chai Lawrence F Bielak Yasuharu Tabara Yang Hai Gudmar Thorleifsson Niels Grarup Tamar Sofer Matthias Wuttke Chloé Sarnowski Christian Gieger Darryl Nousome Stella Trompet Soo-Heon Kwak Jirong Long Meng Sun Lin Tong Wei-Min Chen Suraj S Nongmaithem Raymond Noordam Victor J Y Lim Claudia H T Tam Yoonjung Yoonie Joo Chien-Hsiun Chen Laura M Raffield Bram Peter Prins Aude Nicolas Lisa R Yanek Guanjie Chen Jennifer A Brody Edmond Kabagambe Ping An Anny H Xiang Hyeok Sun Choi Brian E Cade Jingyi Tan K Alaine Broadaway Alice Williamson Zoha Kamali Jinrui Cui Manonanthini Thangam Linda S Adair Adebowale Adeyemo Carlos A Aguilar-Salinas Tarunveer S Ahluwalia Sonia S Anand Alain Bertoni Jette Bork-Jensen Ivan Brandslund Thomas A Buchanan Charles F Burant Adam S Butterworth Mickaël Canouil Juliana C N Chan Li-Ching Chang Miao-Li Chee Ji Chen Shyh-Huei Chen Yuan-Tsong Chen Zhengming Chen Lee-Ming Chuang Mary Cushman John Danesh Swapan K Das H Janaka de Silva George Dedoussis Latchezar Dimitrov Ayo P Doumatey Shufa Du Qing Duan Kai-Uwe Eckardt Leslie S Emery Daniel S Evans Michele K Evans Krista Fischer James S Floyd Ian Ford Oscar H Franco Timothy M Frayling Barry I Freedman Pauline Genter Hertzel C Gerstein Vilmantas Giedraitis Clicerio González-Villalpando Maria Elena González-Villalpando Penny Gordon-Larsen Myron Gross Lindsay A Guare Sophie Hackinger Liisa Hakaste Sohee Han Andrew T Hattersley Christian Herder Momoko Horikoshi Annie-Green Howard Willa Centre for Genetics and Genomics Versus Arthritis Centre for Musculoskeletal Research Division of Musculoskeletal and Dermatological Sciences University of Manchester Manchester UK. Department of Diabetes and Metabolic Diseases Graduate School of Medicine University of Tokyo Tokyo Japan. Department of Statistical Genetics Osaka University Graduate School of Medicine Suita Japan. Institute of Translational Genomics Helmholtz Zentrum München German Research Center for Environmental Health Neuherberg Germany. konstantinos.hatzikotoulas@helmholtz-munich.de. Institute of Translational Genomics Helmholtz Zentrum München German Research Center for Environmental Health Neuherberg Germany. Center for Precision Health Research National Human Genome Research Institute National Institutes of Health Bethesda MD USA. British Heart Foundation Cardiovascular Epidemiology Unit Department of Public Health and Primary Care University of Cambridge Cambridge UK. Heart and Lung Research Institute University of Cambridge Cambridge UK. Department of Epidemiology School of Public Health Nanjing Medical University Nanjing China. Department of Biostatistics and Center for Statistical Genetics University of Michigan Ann Arbor MI USA. Corporal Michael J. Crescenz VA Medical Center Philadelphia PA USA. Department of Systems Pharmacology and Translational Therapeutics University of Pennsylvania Perelman School of Medicine Philadelphia PA USA. Department of Genetics University of Pennsylvania Perelman School of Medicine Philadelphia PA USA. Programs in Metabolism and Medical and Population Genetics Broad Institute of Harvard and MIT Cambridge MA USA. Diabetes Unit and Center for Genomic Medicine Massachusetts General Hospital Boston MA USA. TIMI Study Group Division of Cardiovascular Medicine Brigham and Women's Hospital Harvard Medical School Boston MA USA. William Harvey Research Institute Barts and the London School of Medicine and Dentistry Queen Mary University of London L

Type 2 diabetes (T2D) is a heterogeneous disease that develops through diverse pathophysiological processes and molecular mechanisms that are often specific to cell type. Here, to characterize the genetic contribution to these processes across ancestry groups, we aggregate genome-wide association study data from 2,535,601 individuals (39.7% not of European ancestry), including 428,452 cases of T2D. We identify 1,289 independent association signals at genome-wide significance (P < 5 × 10) that map to 611 loci, of which 145 loci are, to our knowledge, previously unreported. We define eight non-overlapping clusters of T2D signals that are characterized by distinct profiles of cardiometabolic trait associations. These clusters are differentially enriched for cell-type-specific regions of open chromatin, including pancreatic islets, adipocytes, endothelial cells and enteroendocrine cells. We build cluster-specific partitioned polygenic scores in a further 279,552 individuals of diverse ancestry, including 30,288 cases of T2D, and test their association with T2D-related vascular outcomes. Cluster-specific partitioned polygenic scores are associated with coronary artery disease, peripheral artery disease and end-stage diabetic nephropathy across ancestry groups, highlighting the importance of obesity-related processes in the development of vascular outcomes. Our findings show the value of integrating multi-ancestry genome-wide association study data with single-cell epigenomics to disentangle the aetiological heterogeneity that drives the development and progression of T2D. This might offer a route to optimize global access to genetically informed diabetes care.

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Chronic obstructive pulmonary disease and related phenotypes: polygenic risk scores in population-based and case-control cohorts

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The Lancet Respiratory Medicine 2020年第7期8卷 696-708页

作者： Moll, Matthew Sakornsakolpat, Phuwanat Shrine, Nick Hobbs, Brian D DeMeo, Dawn L John, Catherine Guyatt, Anna L McGeachie, Michael J Gharib, Sina A Obeidat, Ma'en Lahousse, Lies Wijnant, Sara R A Brusselle, Guy Meyers, Deborah A Bleecker, Eugene R Li, Xingnan Tal-Singer, Ruth Manichaikul, Ani Rich, Stephen S Won, Sungho Kim, Woo Jin Do, Ah Ra Washko, George R Barr, R Graham Psaty, Bruce M Bartz, Traci M Hansel, Nadia N Barnes, Kathleen Hokanson, John E Crapo, James D Lynch, David Bakke, Per Gulsvik, Amund Hall, Ian P Wain, Louise Soler Artigas, María Jackson, Victoria E Strachan, David P Hui, Jennie James, Alan L Kerr, Shona M Polasek, Ozren Vitart, Veronique Marten, Jonathan Rudan, Igor Kähönen, Mika Surakka, Ida Gieger, Christian Karrasch, Stefan Rawal, Rajesh Schulz, Holger Deary, Ian J Harris, Sarah E Enroth, Stefan Gyllensten, Ulf Imboden, Medea Probst-Hensch, Nicole M Lehtimäki, Terho Raitakari, Olli T Langenberg, Claudia Luan, Jian'an Wareham, Nick Zhao, Jing Hua Hayward, Caroline Murray, Alison Porteous, David J Smith, Blair H Jarvelin, Marjo-Riitta Wielscher, Matthias Joshi, Peter K Kentistou, Katherine A Timmers, Paul RHJ Wilson, James F Cook, James P Lind, Lars Mahajan, Anubha Morris, Andrew P Ewert, Ralf Homuth, Georg Stubbe, Beate Weiss, Stefan Zeggini, Eleftheria Weiss, Scott T Silverman, Edwin K Dudbridge, Frank Tobin, Martin D Cho, Michael H Channing Division of Network Medicine Brigham and Women's Hospital Boston MA United States Division of Pulmonary and Critical Care Medicine Brigham and Women's Hospital Boston MA United States Department of Medicine Faculty of Medicine Siriraj Hospital Mahidol University Bangkok Thailand Genetic Epidemiology Group Department of Health Sciences University of Leicester Leicester United Kingdom Computational Medicine Core Center for Lung Biology Department of Medicine University of Washington Seattle WA United States Division of Pulmonary Critical Care and Sleep Medicine Department of Medicine University of Washington Seattle WA United States Cardiovascular Health Research Unit Department of Medicine University of Washington Seattle WA United States University of British Columbia Center for Heart Lung Innovation St Paul's Hospital Vancouver BC Canada Department of Epidemiology Erasmus Medical Centre Rotterdam Netherlands Department of Respiratory Medicine Erasmus Medical Centre Rotterdam Netherlands Department of Bioanalysis Faculty of Pharmaceutical Sciences Ghent University Ghent Belgium Department of Respiratory Medicine Ghent University Hospital Ghent Belgium Department of Medicine University of Arizona Tucson AZ United States GlaxoSmithKline Research and Development Collegeville PA United States Center for Public Health Genomics University of Virginia Charlottesville VA United States Department of Public Health Sciences University of Virginia Charlottesville VA United States Department of Public Health Sciences Graduate School of Public Health Seoul National University Seoul South Korea Interdisciplinary Program of Bioinformatics College of National Sciences Seoul National University Seoul South Korea Institute of Health and Environment Seoul National University Seoul South Korea Department of Internal Medicine Kangwon National University Chuncheon South Korea Department of Medicine and Department of Epidemiology Columbia Universit

Background: Genetic factors influence chronic obstructive pulmonary disease (COPD) risk, but the individual variants that have been identified have small effects. We hypothesised that a polygenic risk score using additional variants would predict COPD and associated phenotypes. Methods: We constructed a polygenic risk score using a genome-wide association study of lung function (FEV₁ and FEV₁/forced vital capacity [FVC]) from the UK Biobank and SpiroMeta. We tested this polygenic risk score in nine cohorts of multiple ethnicities for an association with moderate-to-severe COPD (defined as FEV₁/FVC <0·7 and FEV₁ <80% of predicted). Associations were tested using logistic regression models, adjusting for age, sex, height, smoking pack-years, and principal components of genetic ancestry. We assessed predictive performance of models by area under the curve. In a subset of studies, we also studied quantitative and qualitative CT imaging phenotypes that reflect parenchymal and airway pathology, and patterns of reduced lung growth. Findings: The polygenic risk score was associated with COPD in European (odds ratio [OR] per SD 1·81 [95% CI 1·74–1·88] and non-European (1·42 [1·34–1·51]) populations. Compared with the first decile, the tenth decile of the polygenic risk score was associated with COPD, with an OR of 7·99 (6·56–9·72) in European ancestry and 4·83 (3·45–6·77) in non-European ancestry cohorts. The polygenic risk score was superior to previously described genetic risk scores and, when combined with clinical risk factors (ie, age, sex, and smoking pack-years), showed improved prediction for COPD compared with a model comprising clinical risk factors alone (AUC 0·80 [0·79–0·81] vs 0·76 [0·75–0·76]). The polygenic risk score was associated with CT imaging phenotypes, including wall area percent, quantitative and qualitative measures of emphysema, local histogram emphysema patterns, and destructive emphysema subtypes. The po

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Gut microbiota composition can reflect immune responses of latent tuberculosis infection in patients with poorly controlled diabetes

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Respiratory research 2023年第1期24卷 11页

作者： Hung-Ling Huang Yong-Chun Luo Po-Liang Lu Cheng-Hsieh Huang Kun-Der Lin Meng-Rui Lee Meng-Hsuan Cheng Yao-Tsung Yeh Cheng-Yuan Kao Jann-Yuan Wang Jinn-Moon Yang Inn-Wen Chong Division of Pulmonary and Critical Care Medicine Kaohsiung Medical University Hospital 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Department of Internal Medicine Kaohsiung Medical University Hospital 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Department of Internal Medicine Kaohsiung Municipal Ta-Tung Hospital 68 Jhonghua 3rd Rd Cianjin District Kaohsiung 80145 Taiwan. Graduate Institute of Medicine College of Medicine Kaohsiung Medical University 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Institute of Bioinformatics and Systems Biology National Yang Ming Chiao Tung University 1001 University Road Hsinchu 30010 Taiwan. Center for Liquid Biopsy and Cohort Kaohsiung Medical University 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Aging and Disease Prevention Research Center Fooyin University 151 Jinxue Rd. Daliao Dist. Kaohsiung 83102 Taiwan. Ph. D. Program in Environmental and Occupational Medicine Kaohsiung Medical University 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Department of Medical Laboratory Science and Biotechnology Fooyin University 151 Jinxue Rd. Daliao Dist. Kaohsiung 83102 Taiwan. Division of Endocrinology and Metabolism Kaohsiung Medical University Hospital 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Department of Internal Medicine National Taiwan University Hospital 7 Chung-Shan South Rd. Zhongzheng Dist. Taipei 100225 Taiwan. Department of Respiratory Therapy Kaohsiung Medical University Hospital 100 Shih-Chuan 1st Road Kaohsiung 80708 Taiwan. Immunology Research Center National Health Research Institutes 35 Keyan Road Zhunan Town Miaoli 35053 Taiwan. Department of Internal Medicine National Taiwan University Hospital 7 Chung-Shan South Rd. Zhongzheng Dist. Taipei 100225 Taiwan. jywang@ntu.edu.tw. Institute of Bioinformatics and Systems Biology National Yang Ming Chiao Tung University 1001 University Road Hsinchu 30010 Taiwan. moon@faculty.nctu.edu.tw. Department of Biologica

BACKGROUND:Diabetes mellitus (DM) is a major risk factor for tuberculosis (TB). Evidence has linked the DM-related dysbiosis of gut microbiota to modifiable host immunity to Mycobacterium tuberculosis infection. However, the crosslinks between gut microbiota composition and immunological effects on the development of latent TB infection (LTBI) in DM patients remain uncertain. METHODS:We prospectively obtained stool, blood samples, and medical records from 130 patients with poorly-controlled DM (pDM), defined as ever having an HbA1c > 9.0% within previous 1 year. Among them, 43 had LTBI, as determined by QuantiFERON-TB Gold in-Tube assay. The differences in the taxonomic diversity of gut microbiota between LTBI and non-LTBI groups were investigated using 16S ribosomal RNA sequencing, and a predictive algorithm was established using a random forest model. Serum cytokine levels were measured to determine their correlations with gut microbiota. RESULTS:Compared with non-LTBI group, the microbiota in LTBI group displayed a similar alpha-diversity but different beta-diversity, featuring decrease of Prevotella_9, Streptococcus, and Actinomyces and increase of Bacteroides, Alistipes, and Blautia at the genus level. The accuracy was 0.872 for the LTBI prediction model using the aforementioned 6 microbiome-based biomarkers. Compared with the non-LTBI group, the LTBI group had a significantly lower serum levels of IL-17F (p = 0.025) and TNF-α (p = 0.038), which were correlated with the abundance of the aforementioned 6 taxa. CONCLUSIONS:The study results suggest that gut microbiome composition maybe associated with host immunity relevant to TB status, and gut microbial signature might be helpful for the diagnosis of LTBI.

关键词： Diabetic mellitus Gut microbiota Immunity Latent tuberculosis infection

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Using species ranges and macroeconomic data to fill the gap in costs of biological invasions

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Nature ecology & evolution 2025年 2025 May 26页

作者： Ismael Soto Pierre Courtois Arman Pili Enrico Tordoni Eléna Manfrini Elena Angulo Céline Bellard Elizabeta Briski Miloš Buřič Ross N Cuthbert Antonín Kouba Melina Kourantidou Rafael L Macêdo Boris Leroy Phillip J Haubrock Franck Courchamp Brian Leung Faculty of Fisheries and Protection of Waters South Bohemian Research Center of Aquaculture and Biodiversity of Hydrocenoses University of South Bohemia in České Budějovice Vodňany Czech Republic. isma-sa@***. CEE-M University of Montpellier CNRS INRAE Instit Agro Montpellier France. School of Biological Sciences Faculty of Science Monash University Clayton Victoria Australia. Institute for Biochemistry and Biology University of Potsdam Potsdam Germany. Department of Botany Institute of Ecology and Earth Science University of Tartu Tartu Estonia. Université Paris-Saclay CNRS AgroParisTech Ecologie Société Evolution Gif sur Yvette France. Unité Biologie des Organismes et Ecosystèmes Aquatiques (BOREA UMR 8067) Muséum national d'Histoire naturelle Sorbonne Université Université de Caen Normandie CNRS IRD Université des Antilles Paris France. Estación Biológica de Doñana CSIC Seville Spain. GEOMAR Helmholtz-Zentrum für Ozeanforschung Kiel Kiel Germany. Faculty of Fisheries and Protection of Waters South Bohemian Research Center of Aquaculture and Biodiversity of Hydrocenoses University of South Bohemia in České Budějovice Vodňany Czech Republic. Institute for Global Food Security School of Biological Sciences Queen's University Belfast Belfast UK. AMURE University of Western Brittany Plouzané France. Department of Sociology Environmental and Business Economics University of Southern Denmark Esbjerg Denmark. Woods Hole Oceanographic Institution Falmouth MA USA. Marine Policy Center Woods Hole MA USA. Graduate Program in Conservation and Ecotourism Federal University of Rio de Janeiro State Rio de Janeiro Brazil. Leibniz Institute of Freshwater Ecology and Inland Fisheries (IGB) Berlin Germany. Institute of Biology Freie Universität Berlin Berlin Germany. Department of River Ecology and Conservation Senckenberg Research Institute and Natural History Museum Frankfurt Gelnhausen Germany. CAMB Center for Applied Mathematics and Bioinformatics Gulf

Biological invasions threaten global biodiversity, human well-being and economies. Many regional and taxonomic syntheses of monetary costs have been produced recently but with important knowledge gaps owing to uneven geographic and taxonomic research intensity. Here we combine species distribution models, macroeconomic data and the InvaCost database to produce the highest resolution spatio-temporal cost estimates currently available to bridge these gaps. From a subset of 162 invasive species with 'highly reliable' documented costs at the national level, our interpolation focuses on countries that have not reported any costs despite the known presence of invasive species. This analysis demonstrates a substantial underestimation, with global costs potentially estimated to be 1,646% higher for these species than previously recorded. This discrepancy was uneven geographically and taxonomically, respectively peaking in Europe and for plants. Our results showed that damage costs were primarily driven by gross domestic product, human population size, agricultural area and environmental suitability, whereas management expenditure correlated with gross domestic product and agriculture areas. We also found a lag time for damage costs of 46 years, but management spending was not delayed. The methodological predictive approach of this study provides a more complete view of the economic dimensions of biological invasions and narrows the global disparity in invasion cost reporting.

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Phosphor-IWS1-dependent U2AF2 splicing regulates trafficking of CAR-E-positive intronless gene mRNAs and sensitivity to viral infection

Communications biology

引用

Communications biology 2021年第1期4卷 1179页

作者： Georgios I Laliotis Adam D Kenney Evangelia Chavdoula Arturo Orlacchio Abdul Kaba Alessandro La Ferlita Vollter Anastas Christos Tsatsanis Joal D Beane Lalit Sehgal Vincenzo Coppola Jacob S Yount Philip N Tsichlis Department of Cancer Biology and Genetics The Ohio State University College of Medicine Columbus Columbus OH 43210 USA. glaliot1@jhmi.edu. The Ohio State University Comprehensive Cancer Center Columbus OH 43210 USA. glaliot1@jhmi.edu. University of Crete School of Medicine Heraklion Crete 71500 Greece. glaliot1@jhmi.edu. Sidney Kimmel Comprehensive Cancer Center and Department of Oncology Johns Hopkins School of Medicine Baltimore MD 21205 USA. glaliot1@jhmi.edu. The Ohio State University Comprehensive Cancer Center Columbus OH 43210 USA. Department of Microbial Infection and Immunity and Infectious Diseases Institute The Ohio State University Columbus OH 43210 USA. Department of Cancer Biology and Genetics The Ohio State University College of Medicine Columbus Columbus OH 43210 USA. Department of Clinical and Experimental Medicine Bioinformatics Unit University of Catania Catania 95131 Italy. Tufts Graduate School of Biomedical Sciences Program in Genetics Boston MA 02111 USA. University of Crete School of Medicine Heraklion Crete 71500 Greece. Institute of Molecular Biology and Biotechnology Heraklion Crete 70013 Greece. Department of Surgery Division of Surgical Oncology Columbus OH 43210 USA. Department of Medicine Division of Hematology The Ohio State University Columbus OH 43210 USA. Department of Cancer Biology and Genetics The Ohio State University College of Medicine Columbus Columbus OH 43210 USA. Philip.tsichlis@osumc.edu. The Ohio State University Comprehensive Cancer Center Columbus OH 43210 USA. Philip.tsichlis@osumc.edu. Tufts Graduate School of Biomedical Sciences Program in Genetics Boston MA 02111 USA. Philip.tsichlis@osumc.edu.

AKT-phosphorylated IWS1 promotes Histone H3K36 trimethylation and alternative RNA splicing of target genes, including the U2AF65 splicing factor-encoding U2AF2. The predominant U2AF2 transcript, upon IWS1 phosphorylation block, lacks the RS-domain-encoding exon 2, and encodes a protein which fails to bind Prp19. Here we show that although both U2AF65 isoforms bind intronless mRNAs containing cytoplasmic accumulation region elements (CAR-E), only the RS domain-containing U2AF65 recruits Prp19 and promotes their nuclear export. The loading of U2AF65 to CAR-Elements was RS domain-independent, but RNA PolII-dependent. Virus- or poly(I:C)-induced type I IFNs are encoded by genes targeted by the pathway. IWS1 phosphorylation-deficient cells therefore, express reduced levels of IFNα1/IFNβ1 proteins, and exhibit enhanced sensitivity to infection by multiple cytolytic viruses. Enhanced sensitivity of IWS1-deficient cells to Vesicular Stomatitis Virus and Reovirus resulted in enhanced apoptotic cell death via caspase activation. Inhibition of this pathway may therefore sensitize cancer cells to oncolytic viruses.

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