41 research outputs found

    Relation of circulating concentrations of chemokine receptor CCR5 ligands to C-peptide, proinsulin and HbA1c and disease progression in type 1 diabetes

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    Th1 related chemokines CCL3 and CCL5 and Th2 related CCL4 as ligands of the receptor CCR5 contribute to disease development in animal models of type 1 diabetes. In humans, no data are available addressing the role of these chemokines regarding disease progression and remission. We investigated longitudinally circulating concentrations of CCR5 ligands of 256 newly diagnosed patients with type 1 diabetes. CCR5 ligands were differentially associated with beta-cell function and clinical remission. CCL5 was decreased in remitters and positively associated with HbA1c suggestive of a Th1 associated progression of the disease. Likewise, CCL3 was negatively related to C-peptide and positively associated with the beta-cell stress marker proinsulin but increased in remitters. CCL4 associated with decreased beta-cell stress shown by negative association with proinsulin. Blockage of chemokines or antagonism of CCR5 by therapeutic agents such as maraviroc may provide a new therapeutic target to ameliorate disease progression in type 1 diabetes

    Development and validation of a weather-based model for predicting infection of loquat fruit by Fusicladium eriobotryae

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    A mechanistic, dynamic model was developed to predict infection of loquat fruit by conidia of Fusicladium eriobotryae, the causal agent of loquat scab. The model simulates scab infection periods and their severity through the sub-processes of spore dispersal, infection, and latency (i.e., the state variables); change from one state to the following one depends on environmental conditions and on processes described by mathematical equations. Equations were developed using published data on F. eriobotryae mycelium growth, conidial germination, infection, and conidial dispersion pattern. The model was then validated by comparing model output with three independent data sets. The model accurately predicts the occurrence and severity of infection periods as well as the progress of loquat scab incidence on fruit (with concordance correlation coefficients .0.95). Model output agreed with expert assessment of the disease severity in seven loquatgrowing seasons. Use of the model for scheduling fungicide applications in loquat orchards may help optimise scab management and reduce fungicide applications.This work was funded by Cooperativa Agricola de Callosa d'En Sarria (Alicante, Spain). Three months' stay of E. Gonzalez-Dominguez at the Universita Cattolica del Sacro Cuore (Piacenza, Italy) was supported by the Programa de Apoyo a la Investigacion y Desarrollo (PAID-00-12) de la Universidad Politecnica de Valencia. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.González Domínguez, E.; Armengol Fortí, J.; Rossi, V. (2014). Development and validation of a weather-based model for predicting infection of loquat fruit by Fusicladium eriobotryae. PLoS ONE. 9(9):1-12. https://doi.org/10.1371/journal.pone.0107547S11299Sánchez-Torres, P., Hinarejos, R., & Tuset, J. J. (2009). Characterization and Pathogenicity ofFusicladium eriobotryae, the Fungal Pathogen Responsible for Loquat Scab. Plant Disease, 93(11), 1151-1157. doi:10.1094/pdis-93-11-1151Gladieux, P., Caffier, V., Devaux, M., & Le Cam, B. (2010). Host-specific differentiation among populations of Venturia inaequalis causing scab on apple, pyracantha and loquat. Fungal Genetics and Biology, 47(6), 511-521. doi:10.1016/j.fgb.2009.12.007González-Domínguez, E., Rossi, V., Armengol, J., & García-Jiménez, J. (2013). Effect of Environmental Factors on Mycelial Growth and Conidial Germination ofFusicladium eriobotryae, and the Infection of Loquat Leaves. Plant Disease, 97(10), 1331-1338. doi:10.1094/pdis-02-13-0131-reGonzález-Domínguez, E., Rossi, V., Michereff, S. J., García-Jiménez, J., & Armengol, J. (2014). Dispersal of conidia of Fusicladium eriobotryae and spatial patterns of scab in loquat orchards in Spain. European Journal of Plant Pathology, 139(4), 849-861. doi:10.1007/s10658-014-0439-0Becker, C. M. (1994). Discontinuous Wetting and Survival of Conidia ofVenturia inaequalison Apple Leaves. Phytopathology, 84(4), 372. doi:10.1094/phyto-84-372Hartman, J. R., Parisi, L., & Bautrais, P. (1999). Effect of Leaf Wetness Duration, Temperature, and Conidial Inoculum Dose on Apple Scab Infections. Plant Disease, 83(6), 531-534. doi:10.1094/pdis.1999.83.6.531Holb, I. J., Heijne, B., Withagen, J. C. M., & Jeger, M. J. (2004). Dispersal of Venturia inaequalis Ascospores and Disease Gradients from a Defined Inoculum Source. Journal of Phytopathology, 152(11-12), 639-646. doi:10.1111/j.1439-0434.2004.00910.xRossi, V., Giosue, S., & Bugiani, R. (2003). Influence of Air Temperature on the Release of Ascospores of Venturia inaequalis. Journal of Phytopathology, 151(1), 50-58. doi:10.1046/j.1439-0434.2003.00680.xStensvand, A., Gadoury, D. M., Amundsen, T., Semb, L., & Seem, R. C. (1997). Ascospore Release and Infection of Apple Leaves by Conidia and Ascospores ofVenturia inaequalisat Low Temperatures. Phytopathology, 87(10), 1046-1053. doi:10.1094/phyto.1997.87.10.1046Machardy WE (1996) Apple scab. Biology, epidemiology and management. St. Paul: APS Press. 545.James, J. R. (1982). Environmental Factors Influencing Pseudothecial Development and Ascospore Maturation ofVenturia inaequalis. Phytopathology, 72(8), 1073. doi:10.1094/phyto-72-1073Li, B., Zhao, H., Li, B., & Xu, X.-M. (2003). Effects of temperature, relative humidity and duration of wetness period on germination and infection by conidia of the pear scab pathogen (Venturia nashicola). Plant Pathology, 52(5), 546-552. doi:10.1046/j.1365-3059.2003.00887.xLi, B.-H., Xu, X.-M., Li, J.-T., & Li, B.-D. (2005). Effects of temperature and continuous and interrupted wetness on the infection of pear leaves by conidia of Venturia nashicola. Plant Pathology, 54(3), 357-363. doi:10.1111/j.1365-3059.2005.01207.xUMEMOTO, S. (1990). Dispersion of ascospores and conidia of causal fungus of Japanese pear scab, Venturia nashicola. Japanese Journal of Phytopathology, 56(4), 468-473. doi:10.3186/jjphytopath.56.468Rossi, V., Salinari, F., Pattori, E., Giosuè,, S., & Bugiani, R. (2009). Predicting the Dynamics of Ascospore Maturation ofVenturia pirinaBased on Environmental Factors. Phytopathology, 99(4), 453-461. doi:10.1094/phyto-99-4-0453Spotts, R. A. (1991). Effect of Temperature and Wetness on Infection of Pear byVenturia pirinaand the Relationship Between Preharvest Inoculation and Storage Scab. Plant Disease, 75(12), 1204. doi:10.1094/pd-75-1204Spotts, R. A. (1994). Factors Affecting Maturation and Release of Ascospores ofVenturia pirinain Oregon. Phytopathology, 84(3), 260. doi:10.1094/phyto-84-260Villalta, O., Washington, W. S., Rimmington, G. M., & Taylor, P. A. (2000). Australasian Plant Pathology, 29(4), 255. doi:10.1071/ap00048Villalta, O. N., Washington, W. S., Rimmington, G. M., & Taylor, P. A. (2000). Effects of temperature and leaf wetness duration on infection of pear leaves by Venturia pirina. Australian Journal of Agricultural Research, 51(1), 97. doi:10.1071/ar99068Lan, Z., & Scherm, H. (2003). Moisture Sources in Relation to Conidial Dissemination and Infection byCladosporium carpophilumWithin Peach Canopies. Phytopathology, 93(12), 1581-1586. doi:10.1094/phyto.2003.93.12.1581Lawrence, Jr., E. G. (1982). Environmental Effects on the Development and Dissemination ofCladosporium carpophilumon Peach. Phytopathology, 72(7), 773. doi:10.1094/phyto-72-773Gottwald, T. R. (1985). Influence of Temperature, Leaf Wetness Period, Leaf Age, and Spore Concentration on Infection of Pecan Leaves by Conidia ofCladosporium caryigenum. Phytopathology, 75(2), 190. doi:10.1094/phyto-75-190Latham, A. J. (1982). Effects of Some Weather Factors andFusicladium effusumConidium Dispersal on Pecan Scab Occurrence. Phytopathology, 72(10), 1339. doi:10.1094/phyto-72-1339MARZO, L., FRISULLO, S., LOPS, F., & ROSSI, V. (1993). Possible dissemination of Spilocaea oleagina conidia by insects (Ectopsocus briggsi). EPPO Bulletin, 23(3), 389-391. doi:10.1111/j.1365-2338.1993.tb01341.xLOPS, F., FRISULLO, S., & ROSSI, V. (1993). Studies on the spread of the olive scab pathogen, Spilocaea oleagina. EPPO Bulletin, 23(3), 385-387. doi:10.1111/j.1365-2338.1993.tb01340.xObanor, F. O., Walter, M., Jones, E. E., & Jaspers, M. V. (2007). Effect of temperature, relative humidity, leaf wetness and leaf age on Spilocaea oleagina conidium germination on olive leaves. European Journal of Plant Pathology, 120(3), 211-222. doi:10.1007/s10658-007-9209-6Obanor, F. O., Walter, M., Jones, E. E., & Jaspers, M. V. (2010). Effects of temperature, inoculum concentration, leaf age, and continuous and interrupted wetness on infection of olive plants by Spilocaea oleagina. Plant Pathology, 60(2), 190-199. doi:10.1111/j.1365-3059.2010.02370.xViruega, J. R., Moral, J., Roca, L. F., Navarro, N., & Trapero, A. (2013). Spilocaea oleaginain Olive Groves of Southern Spain: Survival, Inoculum Production, and Dispersal. Plant Disease, 97(12), 1549-1556. doi:10.1094/pdis-12-12-1206-reViruega, J. R., Roca, L. F., Moral, J., & Trapero, A. (2011). Factors Affecting Infection and Disease Development on Olive Leaves Inoculated withFusicladium oleagineum. Plant Disease, 95(9), 1139-1146. doi:10.1094/pdis-02-11-0126Eikemo, H., Gadoury, D. M., Spotts, R. A., Villalta, O., Creemers, P., Seem, R. C., & Stensvand, A. (2011). Evaluation of Six Models to Estimate Ascospore Maturation in Venturia pyrina. Plant Disease, 95(3), 279-284. doi:10.1094/pdis-02-10-0125Li, B.-H., Yang, J.-R., Dong, X.-L., Li, B.-D., & Xu, X.-M. (2007). A dynamic model forecasting infection of pear leaves by conidia of Venturia nashicola and its evaluation in unsprayed orchards. European Journal of Plant Pathology, 118(3), 227-238. doi:10.1007/s10658-007-9138-4Rossi, V., Giosuè, S., & Bugiani, R. (2007). A-scab (Apple-scab), a simulation model for estimating risk of Venturia inaequalis primary infections. EPPO Bulletin, 37(2), 300-308. doi:10.1111/j.1365-2338.2007.01125.xXU, X.-M., BUTT, D. J., & SANTEN, G. (1995). A dynamic model simulating infection of apple leaves by Venturia inaequalis. Plant Pathology, 44(5), 865-876. doi:10.1111/j.1365-3059.1995.tb02746.xRoubal, C., Regis, S., & Nicot, P. C. (2012). Field models for the prediction of leaf infection and latent period ofFusicladium oleagineumon olive based on rain, temperature and relative humidity. Plant Pathology, 62(3), 657-666. doi:10.1111/j.1365-3059.2012.02666.xPayne, A. F., & Smith, D. L. (2012). Development and Evaluation of Two Pecan Scab Prediction Models. Plant Disease, 96(9), 1358-1364. doi:10.1094/pdis-03-11-0202-reTrapman M, Jansonius PJ (2008) Disease management in organic apple orchards is more than applying the right product at the correct time. Ecofruit-13th International Conference on Cultivation Technique and Phytopathological Problems in Organic Fruit-Growing: Proceedings to the Conference from 18th February to 20th February 2008 at Weinsberg/Germany. 16–22.HOLB, I. J., JONG, P. F., & HEIJNE, B. (2003). Efficacy and phytotoxicity of lime sulphur in organic apple production. Annals of Applied Biology, 142(2), 225-233. doi:10.1111/j.1744-7348.2003.tb00245.xGent, D. H., Mahaffee, W. F., McRoberts, N., & Pfender, W. F. (2013). The Use and Role of Predictive Systems in Disease Management. Annual Review of Phytopathology, 51(1), 267-289. doi:10.1146/annurev-phyto-082712-102356Alavanja, M. C. R., Hoppin, J. A., & Kamel, F. (2004). Health Effects of Chronic Pesticide Exposure: Cancer and Neurotoxicity. Annual Review of Public Health, 25(1), 155-197. doi:10.1146/annurev.publhealth.25.101802.123020Brent KJ, Hollomon DW (2007) Fungicide resistance in crop pathogens: How can it be managed? FRAC Monog 2. Fungicide Resistance Action Committee.Shtienberg, D. (2013). Will Decision-Support Systems Be Widely Used for the Management of Plant Diseases? Annual Review of Phytopathology, 51(1), 1-16. doi:10.1146/annurev-phyto-082712-102244Leffelaar P (1993) On Systems Analysis and Simulation of Ecological Processes. Kluwer. London.Rossi V, Giosuè S, Caffi T (2010) Modelling plant diseases for decision making in crop protection. In: Oerke E-C, Gerhards R, Menz G, Sikora RA, editors. Precision Crop Protection-the Challenge and Use of Heterogeneity.Hui, C. (2006). Carrying capacity, population equilibrium, and environment’s maximal load. Ecological Modelling, 192(1-2), 317-320. doi:10.1016/j.ecolmodel.2005.07.001Townsend C, Begon M, Harper J (2008) Essentials of ecology. John Wiley and Sons. New York. 510.Zadoks J, Schein R (1979) Epidemiology and plant disease management. Oxford University Press, New York. 427.Bennett, J. C., Diggle, A., Evans, F., & Renton, M. (2013). Assessing eradication strategies for rain-splashed and wind-dispersed crop diseases. Pest Management Science, 69(8), 955-963. doi:10.1002/ps.3459Ghanbarnia, K., Dilantha Fernando, W. G., & Crow, G. (2009). Developing Rainfall- and Temperature-Based Models to Describe Infection of Canola Under Field Conditions Caused by Pycnidiospores of Leptosphaeria maculans. Phytopathology, 99(7), 879-886. doi:10.1094/phyto-99-7-0879Gilligan, C. A., & van den Bosch, F. (2008). Epidemiological Models for Invasion and Persistence of Pathogens. Annual Review of Phytopathology, 46(1), 385-418. doi:10.1146/annurev.phyto.45.062806.094357Buck, A. L. (1981). New Equations for Computing Vapor Pressure and Enhancement Factor. Journal of Applied Meteorology, 20(12), 1527-1532. doi:10.1175/1520-0450(1981)0202.0.co;2Madden L V, Hughes G, van den Bosch F (2007) The study of plant disease epidemics. APS press. St. Paul. 421.González-Domínguez E, Rodríguez-Reina J, García-Jiménez J, Armengol J (2014) Evaluation of fungicides to control loquat scab caused by Fusicladium eriobotryae. Plant Heal Prog Accepted.De Wolf, E. D., & Isard, S. A. (2007). Disease Cycle Approach to Plant Disease Prediction. Annual Review of Phytopathology, 45(1), 203-220. doi:10.1146/annurev.phyto.44.070505.143329Krause, R. A., & Massie, L. B. (1975). Predictive Systems: Modern Approaches to Disease Control. Annual Review of Phytopathology, 13(1), 31-47. doi:10.1146/annurev.py.13.090175.000335Fourie, P., Schutte, T., Serfontein, S., & Swart, F. (2013). Modeling the Effect of Temperature and Wetness on Guignardia Pseudothecium Maturation and Ascospore Release in Citrus Orchards. Phytopathology, 103(3), 281-292. doi:10.1094/phyto-07-11-0194Gadoury, D. M. (1982). A Model to Estimate the Maturity of Ascospores ofVenturia inaequalis. Phytopathology, 72(7), 901. doi:10.1094/phyto-72-901Holtslag, Q. A., Remphrey, W. R., Fernando, W. G. D., St-Pierre, R. G., & Ash, G. H. B. (2004). The development of a dynamic diseaseforecasting model to controlEntomosporium mespilionAmelanchier alnifolia. Canadian Journal of Plant Pathology, 26(3), 304-313. doi:10.1080/07060660409507148Legler SEE, Caffi T, Rossi V (2013) A Model for the development of Erysiphe necator chasmothecia in vineyards. Plant Pathol. DOI:10.1111/ppa.12145.Luo, Y., & Michailides, T. J. (2001). Risk Analysis for Latent Infection of Prune by Monilinia fructicola in California. Phytopathology, 91(12), 1197-1208. doi:10.1094/phyto.2001.91.12.1197Gadoury, D. M. (1986). Forecasting Ascospore Dose of Venturia inaequalis in Commercial Apple Orchards. Phytopathology, 76(1), 112. doi:10.1094/phyto-76-112Gent, D. H., De Wolf, E., & Pethybridge, S. J. (2011). Perceptions of Risk, Risk Aversion, and Barriers to Adoption of Decision Support Systems and Integrated Pest Management: An Introduction. Phytopathology, 101(6), 640-643. doi:10.1094/phyto-04-10-0124Schut, M., Rodenburg, J., Klerkx, L., van Ast, A., & Bastiaans, L. (2014). Systems approaches to innovation in crop protection. A systematic literature review. Crop Protection, 56, 98-108. doi:10.1016/j.cropro.2013.11.017Mills W, Laplante A (1954) Diseases and insect in the orchard. Cornell Ext Bull 711.GVA (2013) Octubre-Noviembre 2013. Butlletí d’avisos 13.MacHardy, W. E. (1989). A Revision of Mills’s Criteria for Predicting Apple Scab Infection Periods. Phytopathology, 79(3), 304. doi:10.1094/phyto-79-30

    Non-target impact of fungicide tetraconazole on microbial communities in soils with different agricultural management

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    Effect of the fungicide tetraconazole on microbial community in silt loam soils from orchard with long history of triazole application and from grassland with no known history of fungicide usage was investigated. Triazole tetraconazole that had never been used on these soils before was applied at the field rate and at tenfold the FR. Response of microbial communities to tetraconazole was investigated during 28-day laboratory experiment by determination of changes in their biomass and structure (phospholipid fatty acids method—PLFA), activity (fluorescein diacetate hydrolysis—FDA) as well as changes in genetic (DGGE) and functional (Biolog) diversity. Obtained results indicated that the response of soil microorganisms to tetraconazole depended on the management of the soils. DGGE patterns revealed that both dosages of fungicide affected the structure of bacterial community and the impact on genetic diversity and richness was more prominent in orchard soil. Values of stress indices—the saturated/monounsaturated PLFAs ratio and the cyclo/monounsaturated precursors ratio, were almost twice as high and the Gram-negative/Gram-positive ratio was significantly lower in the orchard soil compared with the grassland soil. Results of principal component analysis of PLFA and Biolog profiles revealed significant impact of tetraconazole in orchard soil on day 28, whereas changes in these profiles obtained for grassland soil were insignificant or transient. Obtained results indicated that orchards soil seems to be more vulnerable to tetraconazole application compared to grassland soil. History of pesticide application and agricultural management should be taken into account in assessing of environmental impact of studied pesticides. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s10646-016-1661-7) contains supplementary material, which is available to authorized users

    Abnormalities of the stigma of sour cherry cultivar

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    The objective of this study was to evaluate the ratio of blackness of the surface of stigma of sour cherry cultivars. At the full bloom time of sour cherry 100 new opened flowers were marked in the internal (Inside), external (outside), bottom and upper parts of the crown of each cultivars including sour cherry cultivars ‘Érdi bőtermő', `Debreceni bőtermő', `Kántorjánosi', 'R. clone', 'Petri', Pándy', and 'D. clone'. The trees were replicated four times. The numbers of flowers with black stigma were counted and the percentage of dead stigma was calculated. In addition, tissues of black stigmata were investigated for blossom pathogens by microscopy. After flowering time the fruit set of the marked flowers counted and then percentage fruit set was calculated. Numbers of counted flowers were between 300 and 980 depending on the four position of the tree. Black color of stigma could be seen only on three cultivars (`Debreceni bőtermő', Érdi bőtermő' and 'Petri') out of seven assessed cultivars. The highest numbers of black colored stigma were found on cultivar ‘Érdi bőtermő' which ranged between incidences of 12 and 21%. Black stigma was never able to produce a fruit set. Microscopic examination revealed no pathogens associated with black stigma. Different part of the tree resulted different amount of black stigma. Black stigma was the largest on the outer part of the tree on cv. 'Érdi bőtermő' but also bottom part of the tree also produced larger number of black stigma on cvs. `Debreceni bőtermő' and ‘Érdi bőtermő'. Though symptoms were not typical to frost damage, we believe that black stigma is probably due to environmental factors during flowering. This might be associated with late spring cold coming from the soil surface as the bottom and outer part of the tree was more suffered from the disease

    Abnormalities of the stigma of sour cherry cultivar

    No full text
    The objective of this study was to evaluate the ratio of blackness of the surface of stigma of sour cherry cultivars. At the full bloom time of sour cherry 100 new opened flowers were marked in the internal (Inside), external (outside), bottom and upper parts of the crown of each cultivars including sour cherry cultivars ‘Érdi bőtermő', `Debreceni bőtermő', `Kántorjánosi', 'R. clone', 'Petri', Pándy', and 'D. clone'. The trees were replicated four times. The numbers of flowers with black stigma were counted and the percentage of dead stigma was calculated. In addition, tissues of black stigmata were investigated for blossom pathogens by microscopy. After flowering time the fruit set of the marked flowers counted and then percentage fruit set was calculated. Numbers of counted flowers were between 300 and 980 depending on the four position of the tree. Black color of stigma could be seen only on three cultivars (`Debreceni bőtermő', Érdi bőtermő' and 'Petri') out of seven assessed cultivars. The highest numbers of black colored stigma were found on cultivar ‘Érdi bőtermő' which ranged between incidences of 12 and 21%. Black stigma was never able to produce a fruit set. Microscopic examination revealed no pathogens associated with black stigma. Different part of the tree resulted different amount of black stigma. Black stigma was the largest on the outer part of the tree on cv. 'Érdi bőtermő' but also bottom part of the tree also produced larger number of black stigma on cvs. `Debreceni bőtermő' and ‘Érdi bőtermő'. Though symptoms were not typical to frost damage, we believe that black stigma is probably due to environmental factors during flowering. This might be associated with late spring cold coming from the soil surface as the bottom and outer part of the tree was more suffered from the disease
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