Relevant bibliographies by topics / Disease cycle

Academic literature on the topic 'Disease cycle'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Disease cycle"

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De Wolf, Erick D., and Scott A. Isard. "Disease Cycle Approach to Plant Disease Prediction." Annual Review of Phytopathology 45, no. 1 (September 8, 2007): 203–20. http://dx.doi.org/10.1146/annurev.phyto.44.070505.143329.

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Musacchio, Andrea, and Kristian Helin. "Cell cycle, differentiation and disease." Current Opinion in Cell Biology 25, no. 6 (December 2013): 673–75. http://dx.doi.org/10.1016/j.ceb.2013.09.003.

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Dwyer, Barney, Atsushi Takeda, Xiongwei Zhu, George Perry, and Mark Smith. "Ferric Cycle Activity and Alzheimer Disease." Current Neurovascular Research 2, no. 3 (July 1, 2005): 261–67. http://dx.doi.org/10.2174/1567202054368371.

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Grange, John, and Alimuddin Zumla. "Tuberculosis and the poverty-disease cycle." Journal of the Royal Society of Medicine 92, no. 3 (March 1999): 105–7. http://dx.doi.org/10.1177/014107689909200301.

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NABEL, E. G., M. BOEHM, L. M. AKYUREK, T. YOSHIMOTO, M. F. CROOK, M. OLIVE, H. SAN, and X. QU. "Cell Cycle Signaling and Cardiovascular Disease." Cold Spring Harbor Symposia on Quantitative Biology 67 (January 1, 2002): 163–70. http://dx.doi.org/10.1101/sqb.2002.67.163.

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Shankland, Stuart J. "Cell-cycle control and renal disease." Kidney International 52, no. 2 (August 1997): 294–308. http://dx.doi.org/10.1038/ki.1997.335.

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Baehr, Wolfgang, Samuel M. Wu, Alan C. Bird, and Krzysztof Palczewski. "The retinoid cycle and retina disease." Vision Research 43, no. 28 (December 2003): 2957–58. http://dx.doi.org/10.1016/j.visres.2003.10.001.

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Doobin, David J., Tiago J. Dantas, and Richard B. Vallee. "Microcephaly as a cell cycle disease." Cell Cycle 16, no. 3 (November 16, 2016): 247–48. http://dx.doi.org/10.1080/15384101.2016.1252591.

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Shankland, Stuart J. "Cell Cycle Proteins in Glomerular Disease." Kidney and Blood Pressure Research 21, no. 2-4 (1998): 213–14. http://dx.doi.org/10.1159/000025857.

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Griffin, Si�n V., Raimund Pichler, Mary Dittrich, Raghu Durvasula, and Stuart J. Shankland. "Cell cycle control in glomerular disease." Springer Seminars in Immunopathology 24, no. 4 (May 1, 2003): 441–57. http://dx.doi.org/10.1007/s00281-003-0120-8.

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Dissertations / Theses on the topic "Disease cycle"

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Hong, Angela M. "Cell cycle protein expression in AIDS-related and classical Kaposi's sarcoma." Connect to full text, 2004. http://hdl.handle.net/2123/583.

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Thesis (Ph. D.)--University of Sydney, 2004.
Title from title screen (viewed 5 May 2008). Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Faculty of Medicine. Includes list of published articles and presentations. Includes bibliographical references. Also available in print form.
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Uebayashi(Yoshitoshi), Elena Yukie. "Modelling urea-cycle disorder citrullinemia type 1 with disease-specific iPSCs." Kyoto University, 2017. http://hdl.handle.net/2433/227584.

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Hamana, Katy. "An exploration of the physical activity life cycle in Huntington's disease." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/107624/.

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This study aimed to explore how living with Huntington’s disease (HD) impacts on the experience of physical activity (PA) across the stages of the disease. The research questions were: 1) What are the experiences of PA participation across the stages of HD? 2) How do the nuances of living with a neurodegenerative disease such as HD affect engagement in PA? The focus group (FG) method was used to explore the breadth of experiences of PA in the context of HD. Participants of eight FGs across the UK included people across the spectrum of HD with varying degrees of symptom manifestation, caregivers (family members/formal caregivers), and healthcare professionals. Framework analysis method (Ritchie and Spencer 1994) was used for data analyses. The process involved five stages: familiarisation, coding, indexing, charting and mapping, and interpretation of data to develop key themes. A key part of the process was development of an analytical coding framework to use in the indexing (of the data) stage. The data itself and a theoretical model (self-regulation model) were both used to develop the framework. The literature review identified a lack of theoretically underpinned qualitative research in PA and HD, therefore the self-regulation model (SRM) (Levanthal et al. 1984) was selected to explore PA in HD. Components of the SRM were used to develop a priori ‘index codes’ of the framework. Open coding of transcripts was also used to develop ‘index codes’ of the framework. The findings highlighted that over the life-span of the disease the needs and abilities of people with HD change, and this has implications such as coping responses and strategies for how PA is experienced and sustained in HD. Social context and environment are key aspects that require consideration for PA in HD, and this has implications such as consideration of familial or caregiver support and general public awareness of HD for development of management and research interventions. The SRM facilitated understanding of participant experiences, however, it appeared that self-regulation of activities becomes more collaborative with the caregiver as HD progresses. As such, a modified version of the SRM that incorporates the increasingly collaborative regulation of PA has been suggested and is presented for understanding PA in HD.
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Wilks, Mark. "Quantitative bacteriology of the vaginal flora in health and disease." Thesis, Queen Mary, University of London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266015.

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Raina, Arun K. "Oncogenic Parallels in Alzheimer Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=case1102023891.

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Smith, Maria Z. "Neuronal cell cycle regulation and the pathophysiology of Alzheimer's disease and related dementias." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393617.

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Bourgeois, Chantal G. "The impact of AIDS on the life cycle of young gay men." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0022/MQ50697.pdf.

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Chen, Lina. "Structural and functional studies of the cell cycle regulator RGC-32." Thesis, University of Sussex, 2017. http://sro.sussex.ac.uk/id/eprint/68451/.

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Boeras, Debrah I. "Chromosome missegregation in Alzheimer's disease caused by presenilin 1." [Tampa, Fla] : University of South Florida, 2005. http://purl.fcla.edu/usf/dc/et/SFE0001706.

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Dear, Graeme. "Studies on the biology, metabolism and pathogenicity of Pseudomonas Anguilliseptica." Thesis, Heriot-Watt University, 1985. http://hdl.handle.net/10399/1599.

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Books on the topic "Disease cycle"

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Mayerson, Charlotte. The death cycle machine. New York: Crown Publishers, 1995.

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Michigan. Department of Community Health. Genetics through the life cycle: Improving health and preventing disease. 8th ed. Lansing, Mich: Michigan Dept. of Community Health, 2004.

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Okazawa, T. Biting cycle of malaria vectors in Solomon Islands. Honiara, Solomon Islands: Malaria Training and Medical Centre, Ministry of Health and Medical Services, 1990.

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An unbreakable cycle: Drug dependency treatment, mandatory confinement, and HIV/AIDS in China's Guangxi Province. New York, NY: Human Rights Watch, 2008.

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1950-, Karmazyn M., Avkiran M, and Fliegel Larry 1956-, eds. The sodium-hydrogen exchanger: From molecule to its role in disease. Boston: Kluwer Academic Publishers, 2003.

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Lee, D. ITER safety task NID-10A: CANDU occupational exposure experience : ore for ITER fuel cycle & cooling systems. Mississauga, ON: Canadian Fusion Fuels Technology Project, 1995.

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Nawe, Julita. The economic cycle of disease: The case of worker's working conditions with emphasis on women at the Morogoro Leather Goods Co. Ltd., Morogoro, Tanzania. Dar es Salaam [Tanzania]: WRDP, 1990.

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Takahashi, Rikiya, and Hibiki Kai. Handbook of macrophages: Life cycle, functions and diseases. Hauppauge, N.Y: Nova Science Publisher's, 2011.

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Slade, Suzanne. The Phases of the Moon. New York: Rosen Pub. Group's PowerKids Press, 2007.

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Breaking the vicious cycle: Intestinal health through diet. Kirkton, Ontario: Kirkton Press, 1994.

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Book chapters on the topic "Disease cycle"

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Saharan, Govind Singh, Naresh Mehta, and Prabhu Dayal Meena. "Disease Cycle." In Downy Mildew Disease of Crucifers: Biology, Ecology and Disease Management, 175–81. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-7500-1_8.

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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Disease Cycle." In Clubroot Disease of Crucifers, 353–73. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-2133-8_8.

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Williams, Nancy I. "Menstrual Cycle." In Encyclopedia of Exercise Medicine in Health and Disease, 559–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_129.

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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "Reproductive Cycle." In Encyclopedia of Exercise Medicine in Health and Disease, 761. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4501.

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Rappold, Gudrun, John-John B. Schnog, Victor E. A. Gerdes, Yvonne G. Weber, Jose M. Serratosa, Anna-Elina Lehesjoki, Alessandra Baumer, et al. "Urea Cycle Disorders." In Encyclopedia of Molecular Mechanisms of Disease, 2141. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8806.

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Beckerman, Martin. "The Cell Cycle." In Cellular Signaling in Health and Disease, 179–200. New York, NY: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-98173-4_9.

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Singh Saharan, Govind, Naresh Mehta, and Prabhu Dayal Meena. "Infection Process, Pathogenesis and Disease Cycle." In Alternaria Diseases of Crucifers: Biology, Ecology and Disease Management, 87–98. Singapore: Springer Singapore, 2015. http://dx.doi.org/10.1007/978-981-10-0021-8_4.

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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Infection, Pathogenesis, and Disease Cycle." In Powdery Mildew Disease of Crucifers: Biology, Ecology and Disease Management, 95–130. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9853-7_4.

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Tronsmo, Anne Marte, Lisa Munk, Annika Djurle, and David B. Collinge. "The disease cycle and lifestyles." In Plant pathology and plant diseases, 19–35. Wallingford: CABI, 2020. http://dx.doi.org/10.1079/9781789243185.0019.

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Behl, Christian, and Christine Ziegler. "Cell Cycle: The Life Cycle of a Cell." In Cell Aging: Molecular Mechanisms and Implications for Disease, 9–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-45179-9_2.

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Conference papers on the topic "Disease cycle"

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Singh, Gaurav K., Vrutangkumar V. Shah, and Harish J. Palanthandalam-Madapusi. "Diagnosis of Parkinson's disease: A limit cycle approach." In 2013 IEEE International Conference on Control Applications (CCA). IEEE, 2013. http://dx.doi.org/10.1109/cca.2013.6662767.

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Dewanjee, Adharaa Neelim, Quazi Delwar Hossain, and Mohammed Shahriar Arefin. "Temporal Variables Disorder of The Gait Cycle in Parkinson’s Disease." In 2019 1st International Conference on Advances in Science, Engineering and Robotics Technology (ICASERT). IEEE, 2019. http://dx.doi.org/10.1109/icasert.2019.8934576.

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Narasimhan, Lakshmi, Di Wu, and Narinder Gill. "Meta-Analysis of Clinical Cardiovascular Data towards Evidential Reasoning for Cardiovascular Life Cycle Management." In InSITE 2007: Informing Science + IT Education Conference. Informing Science Institute, 2007. http://dx.doi.org/10.28945/3147.

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The cardiovascular disease is one of the serious and life-threatening diseases in the developed world. One aspect of medical treatment is using drugs with blood pressure reducing or cholesterol lowering functions. Importantly, such treatment needs to be individually tailored and is significantly correlated to the particular conditions of individual patients. However, such pathologies and mechanisms are still only under investigation. Several novel and unique computational methods, called meta-analyses techniques, for formatting and analyzing a wide variety of cardiac datasets are discussed in this paper with the aim to building cardiovascular database and related patient life-cycle management services. In this paper we also present an overview of a second order inference engine underlying the meta-analyses, which yields evidenced-based reasoning that is more likely to better assist decision-making on the effectiveness of cardiovascular treatment than what is available currently. Furthermore, the software architecture and other details of such a medical informatics system tailored to cardiovascular disease are also described. Research and development work on this project yields itself to application to many other areas, such as disease control and prevention in Epidemiology, and dietics. The system can therefore make a profound impact to medical informatics.
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Probo Sasongko, Hendrik, Febrika Devi Nanda, and Febi Fitriyati. "COMMUNITY KNOWLEDGE LEVEL ABOUT THE UTILIZATION OF INTEGRATED COACHING POS OF NONCOMUNICBALE DISEASE (POSBINDU PTM) WITH THE PREVALENCE OF NONCOMMUNICABLE DISEASE AT AGE 15 – 59 IN WORKING AREA OF WONOSOBO HEALTH CENTER IN SRONO BANYUWANGI 2018." In THE 4th INTERNATIONAL NURSING CONFERENCE “LIFE CYCLE APPROACH FOR SUCCESSFUL AGING”. Universitas Muhammadiyah Jember, 2019. http://dx.doi.org/10.32528/inc.v0i0.2713.

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Ota, Leo, Hirotaka Uchitomi, Kazuki Suzuki, Michael J. Hove, Satoshi Orimo, and Yoshihiro Miyake. "Relationship between fractal property of gait cycle and severity of Parkinson's disease." In 2011 IEEE/SICE International Symposium on System Integration (SII 2011). IEEE, 2011. http://dx.doi.org/10.1109/sii.2011.6147452.

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Wang, Jing, Ping Chen, Cheng Zhang, and Yi Kang. "Corona Virus Disease 2019 Respiratory Cycle Detection Based on Convolutional Neural Network." In 2021 IEEE Biomedical Circuits and Systems Conference (BioCAS). IEEE, 2021. http://dx.doi.org/10.1109/biocas49922.2021.9644970.

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Atukorala, Kushani, Sharaine Fernando, Nalinda Silva, and Lakmali Amarasiri. "Variation in lung functions and airway inflammatory markers of asthmatics during menstrual cycle." In Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp134.

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Li, Xiaoxing, Mengke Chen, Xiaoyi Xu, Ren Wang, Lixia Xu, Ning Zhang, and Guijun Zhao. "IDDF2019-ABS-0263 Androgen receptor promotes gastric carcinogenesis via upregulating the expression of cell cycle-related kinase." In International Digestive Disease Forum (IDDF) 2019, Hong Kong, 8–9 June 2019. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2019. http://dx.doi.org/10.1136/gutjnl-2019-iddfabstracts.104.

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Ng, W. L., F. Adeeb, A. Sebastian, A. Anjum, M. Brady, M. Gillespie, F. Irwin, B. McCarthy, J. Devlin, and A. Fraser. "AB1163 My behcet’s disease and my menstruation cycle: observation from an irish cohort." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2133.

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Alfonso, María, Pilar Cebollero, Juan Bautista Gáldiz Iturri, Sonia Herrero, Vanesa López, Milagros Antón, and Javier Hueto. "Decisive factors during treadmill and cycle exercise in patients with chronic obstructive pulmonary disease." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa305.

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Reports on the topic "Disease cycle"

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Shtienberg, Dan, William Fry, Amos Dinoor, Thomas Zitter, and Uzi Kafkafi. Reduction in Pesticide Use in Plant Disease Control by Integration of Chemical and Non-Chemical Factors. United States Department of Agriculture, May 1995. http://dx.doi.org/10.32747/1995.7613027.bard.

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The long term goal of this research project was to improve control efficiency of Alternaria diseases while reducing fungicide use, by integration of chemical and non-chemical factors. Non-chemical factors were genotype resistance, age-related resistance and fertilizers. The Specific objectives were: 1) To quantify changes in resistance among genotypes and over time in terms of disease development and specific phases of the disease cycle; 2) To quantify the effects of fertilizers applied to the foliage alone, or in combination with a fungicide, on disease development; 3) To quantify the relative contribution of genotype resistance, age-related resistance and fungicide type to the reduction of disease development; 4) To develop a strategy for integration of chemical and non-chemical factors which will achieve optimal disease suppression. The influence of physiological age of cotton plants and of the individual leaves, on disease incidence and on the rate of lesion expansion of A. macrospora was examined on leaves sampled from the field. Both parameters increased with the physiological age of individual leaves but were not affected by the age of the whole plant. The hypothesis that enrichment of the foliage with nitrogen and potassium may enhance host resistance to Alternaria and thus reduce disease severity, was examined for potato and tomato (A. solani ) and for cotton (A. macrospora ). Under controlled environment conditions, application of urea or KNO3 resulted in some reduction in disease development; however, foliar application of both nutrients (8-10 sprays in total) did not affect Alternaria severity in the field. Systemic fungicides against Alternaria (e.g. , tebuconazole and difenoconazole) are more effective than the commonly used protectant fungicides (e.g. mancozeb and chlorothalonil). Concepts for the integration of genotype resistance, age-related resistances and fungicide for the suppression of Alternaria diseases were developed and evaluated. It was found that reduction in host resistance, with age and among genotypes, can be compensated for by adjusting the intensity of fungicide applications, i.e. by increasing the frequency of sprays and by spraying systemic fungicides towards the end of the season. In, moderately resistant cultivars protection can be achieved by spraying at longer intervals than susceptible cultivars. The concepts for integration were evaluated in field trials for cotton, potatoes and tomatoes. By following these concepts it was possible to save up to five sprays out of 8-10 in a growing season.
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Gafny, Ron, A. L. N. Rao, and Edna Tanne. Etiology of the Rugose Wood Disease of Grapevine and Molecular Study of the Associated Trichoviruses. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575269.bard.

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Rugose wood is a complex disease of grapevines, characterized by modification of the woody cylinder of affected vines. The control of rugose wood is based on the production of healthy propagation material. Detection of rugose wood in grapevines is difficult and expensive: budwood from tested plants is grafted onto sensitive Vitis indicators and the appearance of symptoms is monitored for 3 years. The etiology of rugose wood is complex and has not yet been elucidated. Several elongated clostero-like viruses are consistently found in affected vines; one of them, grapevine virus A (GVA), is closely associated with Kober stem grooving, a component of the rugose wood complex. GVA has a single-stranded RNA genome of 7349 nucleotides, excluding a polyA tail at the 3' terminus. The GVA genome includes five open reading frames (ORFs 1-5). ORF 4, which encodes for the coat protein of GVA, is the only ORF for which the function was determined experimentally. The original objectives of this research were: 1- To produce antisera to the structural and non-structural proteins of GVA and GVB and to use these antibodies to establish an effective detection method. 2- Develop full length infectious cDNA clones of GVA and GVB. 3- Study the roll of GVA and GVB in the etiology of the grapevine rugose wood disease. 4- Determine the function of Trichovirus (now called Vitivirus) encoded genes in the virus life cycle. Each of the ORFs 2, 3, 4 and 5 genes of GVA were cloned and expressed in E. coli and used to produce antisera. Both the CP (ORF 4) and the putative MP (ORF 3) were detected with their corresponding antisera in-GVA infected N. benthamiana and grapevine. The MP was first detected at an early stage of the infection, 6-12 h after inoculation, and the CP 2-3 days after inoculation. The MP could be detected in GVA-infected grapevines that tested negative for CP, both with CP antiserum and with a commercially available ELISA kit. Antisera to ORF 2 and 5 encoded proteins could react with the recombinant proteins but failed to detect both proteins in GVA infected plants. A full-length cDNA clone of grapevine virus A (GVA) was constructed downstream from the bacteriophage T7 RNA polymerase promoter. Capped in vitro transcribed RNA was infectious in N. benthamiana and N. clevelandii plants. Symptoms induced by the RNA transcripts or by the parental virus were indistinguishable. The infectivity of the in vitro-transcribed RNA was confirmed by serological detection of the virus coat and movement proteins and by observation of virions by electron microscopy. The full-length clone was modified to include a gus reporter gene and gus activity was detected in inoculated and systemic leaves of infected plants. Studies of GVA mutants suggests that the coat protein (ORF 4) is essential for cell to cell movement, the putative movement protein (ORF 3) indeed functions as a movement protein and that ORF 2 is not required for virus replication, cell to cell or systemic movement. Attempts to infect grapevines by in-vitro transcripts, by inoculation of cDNA construct in which the virus is derived by the CaMV 35S promoter or by approach grafting with infected N. benthamiana, have so far failed. Studies of the subcellular distribution of GFP fusion with each of ORF 2, 3 and 4 encoded protein showed that the CP fusion protein accumulated as a soluble cytoplasmatic protein. The ORF 2 fusion protein accumulated in cytoplasmatic aggregates. The MP-GFP fusion protein accumulated in a large number of small aggregates in the cytoplasm and could not move from cell to cell. However, in conditions that allowed movement of the fusion protein from cell to cell (expression by a PVX vector or in young immature leaves) the protein did not form cytoplasmatic aggregates but accumulated in the plasmodesmata.
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Powell, Amy, Erin Acquesta, Warren Davis, Jefferey Nichol, Irina Tezaur, Kara Peterson, Susan Rempe, and Jose Huerta. Water Cycle-Driven Infectious Diseases as Multiscale, Reliable, Continuously Updating Water Cycle Sensors. Office of Scientific and Technical Information (OSTI), April 2021. http://dx.doi.org/10.2172/1769797.

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Yeates, Elissa, Kayla Cotterman, and Angela Rhodes. Hydrologic impacts on human health : El Niño Southern Oscillation and cholera. Engineer Research and Development Center (U.S.), January 2020. http://dx.doi.org/10.21079/11681/39483.

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A non-stationary climate imposes considerable challenges regarding potential public health concerns. The El Niño Southern Oscillation (ENSO) cycle, which occurs every 2 to 7 years, correlates positively with occurrences of the waterborne disease cholera. The warm sea surface temperatures and extreme weather associated with ENSO create optimal conditions for breeding the Vibrio cholerae pathogen and for human exposure to the pathogenic waters. This work explored the impacts of ENSO on cholera occurrence rates over the past 50 years by examining annual rates of suspected cholera cases per country in relation to ENSO Index values. This study provides a relationship indicating when hydrologic conditions are optimal for cholera growth, and presents a statistical approach to answer three questions: Are cholera outbreaks more likely to occur in an El Niño year? What other factors impact cholera outbreaks? How will the future climate impact cholera incidence rates as it relates to conditions found in ENSO? Cholera outbreaks from the 1960s to the present are examined focusing on regions of Central and South America, and southern Asia. By examining the predictive relationship between climate variability and cholera, we can draw conclusions about future vulnerability to cholera and other waterborne pathogenic diseases.
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Gelb, Jr., Jack, Yoram Weisman, Brian Ladman, and Rosie Meir. Identification of Avian Infectious Brochitis Virus Variant Serotypes and Subtypes by PCR Product Cycle Sequencing for the Rational Selection of Effective Vaccines. United States Department of Agriculture, December 2003. http://dx.doi.org/10.32747/2003.7586470.bard.

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Objectives 1. Determine the serotypic identities of 40 recent IBV isolates from commercial chickens raised in the USA and Israel. 2. Sequence all IBV field isolates using PCR product cycle sequencing and analyze their S 1 sequence to detennine their homology to other strains in the Genbank and EMBL databases. 3. Select vaccinal strains with the highest S 1 sequence homology to the field isolates and perform challenge of immunity studies in chickens in laboratory trials to detennine level of protection afforded by the vaccines. Background Infectious bronchitis (IB) is a common, economically important disease of the chicken. IB occurs as a respiratory form, associated with airsacculitis, condemnation, and mortality of meat-type broilers, a reproductive form responsible for egg production losses in layers and breeders, and a renal form causing high mortality in broilers and pullets. The causative agent is avian coronavirus infectious bronchitis virus (IBV). Replication of the virus' RNA genome is error-prone and mutations commonly result. A major target for mutation is the gene encoding the spike (S) envelope protein used by the virus to attach and infect the host cell. Mutations in the S gene result in antigenic changes that can lead to the emergence of variant serotypes. The S gene is able to tolerate numerous mutations without compromising the virus' ability to replicate and cause disease. An end result of the virus' "flexibility" is that many strains of IBV are capable of existing in nature. Once formed, new mutant strains, often referred to as variants, are soon subjected to immunological selection so that only the most antigenically novel variants survive in poultry populations. Many novel antigenic variant serotypes and genotypes have been isolated from commercial poultry flocks. Identification of the field isolates of IBV responsible for outbreaks is critical for selecting the appropriate strain(s) for vaccination. Reverse transcriptase polymerase chain reaction (RT-PCR) of the Sl subunit of the envelope spike glycoprotein gene has been a common method used to identify field strains, replacing other time-consuming or less precise tests. Two PCR approaches have been used for identification, restriction fragment length polymorphism (RFLP) and direct automated cycle sequence analysis of a diagnostically relevant hypervariab1e region were compared in our BARD research. Vaccination for IB, although practiced routinely in commercial flocks, is often not protective. Field isolates responsible for outbreaks may be unrelated to the strain(s) used in the vaccination program. However, vaccines may provide varying degrees of cross- protection vs. unrelated field strains so vaccination studies should be performed. Conclusions RFLP and S1 sequence analysis methods were successfully performed using the field isolates from the USA and Israel. Importantly, the S1 sequence analysis method enabled a direct comparison of the genotypes of the field strains by aligning them to sequences in public databases e.g. GenBank. Novel S1 gene sequences were identified in both USA and Israel IBVs but greater diversity was observed in the field isolates from the USA. One novel genotype, characterized in this project, Israel/720/99, is currently being considered for development as an inactivated vaccine. Vaccination with IBV strains in the US (Massachusetts, Arkansas, Delaware 072) or in Israel (Massachusetts, Holland strain) provided higher degrees of cross-protection vs. homologous than heterologous strain challenge. In many cases however, vaccination with two strains (only studies with US strains) produced reasonable cross-protection against heterologous field isolate challenge. Implications S1 sequence analysis provides numerical similarity values and phylogenetic information that can be useful, although by no means conclusive, in developing vaccine control strategies. Identification of many novel S1 genotypes of IBV in the USA is evidence that commercial flocks will be challenged today and in the future with strains unrelated to vaccines. In Israel, monitoring flocks for novel IBV field isolates should continue given the identification of Israel/720/99, and perhaps others in the future. Strains selected for vaccination of commercial flocks should induce cross- protection against unrelated genotypes. Using diverse genotypes for vaccination may result in immunity against unrelated field strains.
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Dickman, Martin B., and Oded Yarden. Characterization of the chorismate mutase effector (SsCm1) from Sclerotinia sclerotiorum. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600027.bard.

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Sclerotinia sclerotiorum is a filamentous fungus (mold) that causes plant disease. It has an extremely wide range of hosts (>400 species) and causes considerable damage (annual multimillion dollar losses) in economically important crops. It has proven difficult to control (culturally or chemically) and host resistance to this fungus has generally been inadequate. It is believed that this fungus occurs in almost every country. Virulence of this aggressive pathogen is bolstered by a wide array of plant cell wall degrading enzymes and various compounds (secondary metabolites) produced by the fungus. It is well established that plant pathogenic fungi secrete proteins and small molecules that interact with host cells and play a critical role in disease development. Such secreted proteins have been collectively designated as “effectors”. Plant resistance against some pathogens can be mediated by recognition of such effectors. Alternatively, effectors can interfere with plant defense. Some such effectors are recognized by the host plant and can culminate in a programmed cell death (PCD) resistant response. During the course of this study, we analyzed an effector in Sclerotiniasclerotiorum. This specific effector, SsCM1 is the protein chorismatemutase, which is an enzyme involved in a pathway which is important in the production of important amino acids, such a Tryptophan. We have characterized the Sclerotiniaeffector, SsCM1, and have shown that inactivation of Sscm1 does not affect fungal vegetative growth, development or production of oxalic acid (one of this fungus’ secondary metabolites associated with disease) production. However, yhis does result in reduced fungal virulence. We show that, unexpectedly, the SsCM1 protein translocates to the host chloroplast, and demonstrated that this process is required for full fungal virulence. We have also determined that the fungal SsCM1 protein can interact with similar proteins produced by the host. In addition, we have shown that the fungal SsCM1 is able to suppress at least some of the effects imposed by reactive oxygen species which are produced as a defense mechanism by the host. Last, but not least, the results of our studies have provided evidence contradicting the current dogma on at least some of the mechanist aspects of how this pathogen infects the host. Contrary to previousons, indicating that this pathogen kills its host by use of metabolites and enzymes that degrade the host tissue (a process called necrotrophy), we now know that at least in the early phases of infection, the fungus interacts with live host tissue (a phenomenon known as biotrophy). Taken together, the results of our studies provide novel insights concerning the mechanistic aspects of Sclerotinia-host interactions. We hope this information will be used to interfere with the disease cycle in a manner that will protect plants from this devastating fungus.
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Ohad, Nir, and Robert Fischer. Regulation of plant development by polycomb group proteins. United States Department of Agriculture, January 2008. http://dx.doi.org/10.32747/2008.7695858.bard.

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Our genetic and molecular studies have indicated that FIE a WD-repeat Polycomb group (PcG) protein takes part in multi-component protein complexes. We have shown that FIE PcG protein represses inappropriate programs of development during the reproductive and vegetative phases of the Arabidopsis life cycle. Moreover, we have shown that FIE represses the expression of key regulatory genes that promote flowering (AG and LFY), embryogenesis (LEC1), and shoot formation (KNAT1). These results suggest that the FIE PcG protein participates in the formation of distinct PcG complexes that repress inappropriate gene expression at different stages of plant development. PcG complexes modulate chromatin compactness by modifying histones and thereby regulate gene expression and imprinting. The main goals of our original project were to elucidate the biological functions of PcG proteins, and to understand the molecular mechanisms used by FIE PcG complexes to repress the expression of its gene targets. Our results show that the PcG complex acts within the central cell of the female gametophyte to maintain silencing of MEA paternal allele. Further more we uncovered a novel example of self-imprinting mechanism by the PgG complex. Based on results obtained in the cures of our research program we extended our proposed goals and elucidated the role of DME in regulating plant gene imprinting. We discovered that in addition to MEA,DME also imprints two other genes, FWA and FIS2. Activation of FWA and FIS2 coincides with a reduction in 5-methylcytosine in their respective promoters. Since endosperm is a terminally differentiated tissue, the methylation status in the FWA and FIS2 promoters does not need to be reestablished in the following generation. We proposed a “One-Way Control” model to highlight differences between plant and animal genomic imprinting. Thus we conclude that DEMETER is a master regulator of plant gene imprinting. Future studies of DME function will elucidate its role in processes and disease where DNA methylation has a key regulatory role both in plants and animals. Such information will provide valuable insight into developing novel strategies to control and improve agricultural traits and overcome particular human diseases.
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Perl, Avichai, Bruce I. Reisch, and Ofra Lotan. Transgenic Endochitinase Producing Grapevine for the Improvement of Resistance to Powdery Mildew (Uncinula necator). United States Department of Agriculture, January 1994. http://dx.doi.org/10.32747/1994.7568766.bard.

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The original objectives are listed below: 1. Design vectors for constitutive expression of endochitinase from Trichoderma harzianum strain P1. Design vectors with signal peptides to target gene expression. 2. Extend transformation/regeneration technology to other cultivars of importance in the U.S. and Israel. 3. Transform cultivars with the endochitinase constructs developed as part of objective 1. A. Characterize foliar powdery mildew resistance in transgenic plants. Background of the topic Conventional breeding of grapevines is a slow and imprecise process. The long generation cycle, large space requirements and poor understanding of grapevine genetics prevent rapid progress. There remains great need to improve existing important cultivars without the loss of identity that follows from hybridization. Powdery mildew (Uncinula necator) is the most important fungal pathogen of grapevines, causing economic losses around the world. Genetic control of powdery mildew would reduce the requirement for chemical or cultural control of the disease. Yet, since the trait is under polygenic control, it is difficult to manipulate through hybridization and breeding. Also, because grapevines are heterozygous and vegetatively propagated cultivar identity is lost in the breeding process. Therefore, there is great need for techniques to produce transgenic versions of established cultivars with heterologous genes conferring disease resistance. Such a gene is now available for control of powdery mildew of grapevines. The protein coded by the Endochitinase gene, derived from Trichoderma harzianum, is very effective in suppressing U. necator growth. The goal of this proposal is to develop transgenic grapevines with this antifungal gene, and to test the effect of this gene on resistance to powdery mildew. Conclusions, achievements and implications Gene transfer technology for grape was developed using commercial cultivars for both wine and table grapes. It paved the way for a new tool in grapevine genetic studies enabling the alteration of specific important traits while maintaining the essential features of existing elite cultivars. Regeneration and transformation technologies were developed and are currently at an advanced stage for USA wine and Israeli seedless cultivars, representing the cutting edge of grape genetic engineering studies worldwide. Transgenic plants produced are tested for powdery mildew resistance in greenhouse and field experiments at both locations. It is our ultimate goal to develop transgenic grapes which will be more efficient and economical for growers to produce, while also providing consumers with familiar products grown with reduced chemical inputs.
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Suescun-Melo, Rodrigo. Commodity booms, dutch disease, and real business cycles in a small open economy: the case of coffee in Colombia. Bogotá, Colombia: Banco de la República, June 1997. http://dx.doi.org/10.32468/be.73.

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Adlakha, Deepi, Jane Clarke, Perla Mansour, and Mark Tully. Walk-along and cycle-along: Assessing the benefits of the Connswater Community Greenway in Belfast, UK. Property Research Trust, 2021. http://dx.doi.org/10.52915/ghcj1777.

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Physical inactivity is a risk factor for numerous chronic diseases, and a mounting global health problem. It is likely that the outdoor physical environment, together with social environmental factors, has a tendency to either promote or discourage physical activity, not least in cities and other urban areas. However, the evidence base on this is sparse, making it hard to identify the best policy interventions to make, at the local or city level. This study seeks to assess the impact of one such intervention, the Connswater Community Greenway CCG), in Belfast, in Northern Ireland, UK. To do that it uses innovative methodologies, ‘Walk-along’ and ‘Cycle-along’ that involve wearable sensors and video footages, to improve our understanding of the impact of the CCG on local residents. The findings suggest that four characteristics of the CCG affect people’s activity and the benefits that the CCG created. These are physical factors, social factors, policy factors and individual factors. Each of these has many elements, with different impacts on different people using the greenway.
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