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Cardiac echocardiogram findings of severe acute respiratory syndrome coronavirus-2-associated multi-system inflammatory syndrome in children – CORRIGENDUM
- Ashraf S. Harahsheh, Anita Krishnan, Roberta L. DeBiasi, Laura J. Olivieri, Christopher Spurney, Mary T. Donofrio, Russell R. Cross, Matthew P. Sharron, Lowell H. Frank, Charles I. Berul, Adam Christopher, Niti Dham, Hemalatha Srinivasalu, Tova Ronis, Karen L. Smith, Jaclyn N. Kline, Kavita Parikh, David Wessel, James E. Bost, Sarah Litt, Ashley Austin, Jing Zhang, Craig A. Sable
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- Journal:
- Cardiology in the Young / Volume 32 / Issue 5 / May 2022
- Published online by Cambridge University Press:
- 31 August 2021, p. 727
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Cardiac echocardiogram findings of severe acute respiratory syndrome coronavirus-2-associated multi-system inflammatory syndrome in children
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- Ashraf S. Harahsheh, Anita Krishnan, Roberta L. DeBiasi, Laura J. Olivieri, Christopher Spurney, Mary T. Donofrio, Russell R. Cross, Matthew P. Sharron, Lowell H. Frank, Charles I. Berul, Adam Christopher, Niti Dham, Hemalatha Srinivasalu, Tova Ronis, Karen L. Smith, Jaclyn N. Kline, Kavita Parikh, David Wessel, James E. Bost, Sarah Litt, Ashley Austin, Jing Zhang, Craig A. Sable
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- Journal:
- Cardiology in the Young / Volume 32 / Issue 5 / May 2022
- Published online by Cambridge University Press:
- 05 August 2021, pp. 718-726
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Background:
A novel paediatric disease, multi-system inflammatory syndrome in children, has emerged during the 2019 coronavirus disease pandemic.
Objectives:To describe the short-term evolution of cardiac complications and associated risk factors in patients with multi-system inflammatory syndrome in children.
Methods:Retrospective single-centre study of confirmed multi-system inflammatory syndrome in children treated from 29 March, 2020 to 1 September, 2020. Cardiac complications during the acute phase were defined as decreased systolic function, coronary artery abnormalities, pericardial effusion, or mitral and/or tricuspid valve regurgitation. Patients with or without cardiac complications were compared with chi-square, Fisher’s exact, and Wilcoxon rank sum.
Results:Thirty-nine children with median (interquartile range) age 7.8 (3.6–12.7) years were included. Nineteen (49%) patients developed cardiac complications including systolic dysfunction (33%), valvular regurgitation (31%), coronary artery abnormalities (18%), and pericardial effusion (5%). At the time of the most recent follow-up, at a median (interquartile range) of 49 (26–61) days, cardiac complications resolved in 16/19 (84%) patients. Two patients had persistent mild systolic dysfunction and one patient had persistent coronary artery abnormality. Children with cardiac complications were more likely to have higher N-terminal B-type natriuretic peptide (p = 0.01), higher white blood cell count (p = 0.01), higher neutrophil count (p = 0.02), severe lymphopenia (p = 0.05), use of milrinone (p = 0.03), and intensive care requirement (p = 0.04).
Conclusion:Patients with multi-system inflammatory syndrome in children had a high rate of cardiac complications in the acute phase, with associated inflammatory markers. Although cardiac complications resolved in 84% of patients, further long-term studies are needed to assess if the cardiac abnormalities (transient or persistent) are associated with major cardiac events.
2 - The rice blast story: from genome sequence to function
- from I - Comparative and functional fungal genomics
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- By R. A. Dean, Center for Integrated Fungal Research Department of Plant Pathology 1200 Partners Building II Box 7251 North Carolina State University Raleigh NC 27695 USA, T. Mitchell, North Carolina State University Department of Plant Pathology Campus Box 7251 Raleigh NC 27695–7251 USA, R. Kulkarni, RTI 3040 Cornwallis Road Research Triangle Park NC 27709 USA, N. Donofrio, North Carolina State University Department of Plant Pathology Campus Box 7251 Raleigh NC 27695–7251 USA, A. Powell, North Carolina State University Department of Plant Pathology Campus Box 7251 Raleigh NC 27695–7251 USA, Y. Y. Oh, North Carolina State University Department of Plant Pathology Campus Box 7251 Raleigh NC 27695–7251 USA, S. Diener, North Carolina State University Department of Plant Pathology Campus Box 7253 Raleigh NC 27695–7253 USA, H. Pan, RTI 3040 Cornwallis Road Research Triangle Park NC 27709 USA, D. Brown, North Carolina State University Department of Plant Pathology Campus Box 7251 Raleigh NC 27695–7251 USA, J. Deng, North Carolina State University Department of Plant Pathology Campus Box 7251 Raleigh NC 27695–7251 USA, I. Carbone, North Carolina State University Department of Plant Pathology Campus Box 7244 Raleigh NC 27695–7244 USA, D. J. Ebbole, Department of Plant Pathology and Microbiology Peterson Building Rm 120 MS# 2132 Texas A&M University College Station TX 77843–2132 USA, M. Thon, Department of Computer Science 320C Peterson Building MS# 2132 Texas A&M University College Station TX 77843–2132 USA, M. L. Farman, Department of Plant Pathology University of Kentucky 1405 Veterans Drive Lexington KY 40546–0312 USA, M. J. Orbach, Department of Plant Pathology University of Arizona Forbes Room 105 PO Box 210036 Tucson AZ 85721–0036 USA, C. Soderlund, Director of Bioinformatics Department of Plant Science 303 Forbes Building Tucson AZ 85721 USA, J-R. Xu, Department of Botany and Plant Pathology 915 West State Street Purdue University West Lafayette IN 47906 USA, Y-H. Lee, Seoul National University School of Agricultural Biotechnology Suwon 441–744 Korea, N. J. Talbot, Department of Biological Sciences University of Exeter Hatherly Laboratories Prince of Wales Road Exeter EX4 4PS UK, S. Coughlan, Agilent Technologies Inc. Little Falls Site 2850 Centerville Road Wilmington DE 19808 USA, J. E. Galagan, The Broad Institute Massachusetts Institute of Technology 77 Massachusetts Avenue Cambridge MA 02139–4307 USA, B. W. Birren, The Broad Institute Massachusetts Institute of Technology 77 Massachusetts Avenue Cambridge MA 02139–4307 USA
- Edited by G. D. Robson, University of Manchester, Pieter van West, University of Aberdeen, Geoffrey Gadd, University of Dundee
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- Exploitation of Fungi
- Published online:
- 05 October 2013
- Print publication:
- 24 May 2007, pp 10-22
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Summary
Introduction
Rice blast disease, caused by the filamentous fungus Magnaporthe grisea, is a serious and recurrent problem in all rice-growing regions of the world (Talbot, 2003; Valent & Chumley, 1991). It is estimated that each year enough rice is destroyed by rice blast disease to feed 60 million people. Control of this disease is difficult; new host-specific forms develop quickly to overcome host resistance and chemical control is typically not cost effective (Ou, 1987). Infections occur when fungal spores land and attach themselves to leaves using a special adhesive released from the tip of each spore (Hamer et al., 1988). The germinating spore develops an appressorium, a specialized infection cell, which generates enormous turgor pressure – up to 8 MPa – that ruptures the leaf cuticle allowing invasion of the underlying leaf tissue (de Jong et al., 1997; Dean, 1997). Subsequent colonization of the leaf produces disease lesions from which the fungus sporulates and spreads to new plants. When rice blast infects young rice seedlings, whole plants often die, while spread of the disease to the stems, nodes or panicle of older plants results in nearly total loss of the rice grain. Recent reports have further shown that the fungus has the capacity to infect plant roots (Sesma & Osbourn, 2004). Different host-limited forms of Magnaporthe also infect a broad range of grass species including wheat, barley and millet.