Resistance of mango cultivar Ubá to Ceratocystis fimbriata depends on the pathogen's physiological variability

2021 ◽  
Vol 143 ◽  
pp. 105560
Author(s):  
Lúcio M.S. Guimarães ◽  
Angélica S. Nunes ◽  
Samuel A. Santos ◽  
Marcos D.V. Resende ◽  
Michelle B. Damacena ◽  
...  
2009 ◽  
Vol 62 ◽  
pp. 402-402
Author(s):  
S.L. Lewthwaite ◽  
P.J. Wright

The predominant diseases of the commercial kumara (Ipomoea batatas) or sweetpotato crop are caused by fungal pathogens The field disease pink rot results from infection by the fungus Sclerotinia sclerotiorum Lesions form on vines but may spread down stems to the roots The widespread nature of this disease in sweetpotato appears peculiar to New Zealand Scurf is a disease caused by Monilochaetes infuscans which occurs in the field but may proliferate amongst stored roots The disease causes a superficial discolouration of the root surface which is mainly cosmetic but can also increase root water loss in storage Infection by Ceratocystis fimbriata produces a disease known as black rot The disease can be transmitted amongst plants at propagation but is particularly rampant amongst roots in storage This disease is readily transmitted and can cause severe economic loss Fusarium oxysporum causes surface rots in stored roots characterised by light to dark brown lesions that tend to be firm dry and superficial The lesions may be circular and centred on wounds caused by insects or mechanical damage at harvest Soft rot caused by Rhizopus stolonifer generally occurs in roots after they are washed and prepared for the market Fungal infection occurs through wounds or bruised tissue producing distinctive tufts of white fungal strands and black spores


1978 ◽  
Vol 42 (5) ◽  
pp. 935-939 ◽  
Author(s):  
Akira TAKEUCHI ◽  
Itaro OGUNI ◽  
Kazuko ÔBA ◽  
Mineo KOJIMA ◽  
Ikuzo URITANI

1891 ◽  
Vol 7 (1) ◽  
pp. 1 ◽  
Author(s):  
B. D. Halsted ◽  
D. G. Fairchild

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Thomas A Kent ◽  
Harriett C Rea ◽  
William Dalmeida ◽  
Roderic H Fabian ◽  
Cenk Ayata ◽  
...  

Introduction: Failures to translate pre-clinical results have been discouraging. We have contended that stroke is too heterogeneous with respect to factors influencing outcome to expect small studies to be balanced. It is not only difficult to control for biological and methodological variability but efforts to improve homogeneity, such as minimizing physiological variability, may render results less applicable to humans. Here, we report a predictive outcome model in experimental stroke which incorporates baseline variability and provides statistical thresholds a treatment must exceed to be efficacious in a broad population. Methods: We generated a mathematical model to predict outcome using transient MCA occlusion in 23 unfasted rats. To create baseline variability, we varied occlusion times from 90-120 min, altered baseline glucose with streptozotocin, and assessed neurological outcome 3 days later with a modified Bederson Score (BS; 0-6 functional measure, 7 death). Statistical surfaces in 3 dimensions were generated using Jacobian matrices flanking the model to provide a screening threshold (1 SD) for comparing new therapies against this model. Results: We successfully generated an outcome model from occlusion time, glucose and BS (Fig; R 2 =.49, p=.0003; middle surface is the model surrounded by ±SD surfaces). Outcome was sensitive to change in glucose and time, suggesting small imbalances in these factors between groups may influence outcome, and hence the perceived efficacy of a new therapeutic intervention. At normoglycemia and 90 mins, the lower surface overlapped with no deficit, indicating it would be difficult to reliably demonstrate benefit under those conditions. Conclusions: These results indicate it is feasible to incorporate biological variability to generate more clinically relevant conditions. The method will be tested with other stroke models and modifiers towards a generalized model to screen for therapies worthy of further study.


2005 ◽  
Vol 30 (5) ◽  
pp. 543-545 ◽  
Author(s):  
Francisco A Ferreira ◽  
Luis A Maffia ◽  
Evander A Ferreira

Desenvolveu-se uma técnica de detecção rápida de Ceratocystis fimbriata em lenho de eucalipto (Eucalyptus spp.) infetado, visualizando-se clamidósporos (aleuroconídios) ao microscópio ótico comum, em vasos do xilema, medula e raios medulares, a partir de cortes histopatológicos à mão livre, feitos com lâmina de barbear, ao microscópio estereoscópico. O tempo médio gasto para a detecção do patógeno, do corte histopatológico tangencial à total visualização dos clamidósporos ao microscópio ótico comum, foi de 3,5 min e bem menos utilizando-se corte longitudinal passando pela medula, contra, no mínimo, quatro a cinco dias, usando-se outras técnicas como o isolamento em BDA, deposição de fragmentos de lenho doente entre fatias de cenoura usadas como isca, ou pedaços de lenhos doentes deixados em câmara úmida. Essa técnica histopatológica é também viável para a detecção do patógeno em outros hospedeiros lenhosos e, inclusive, para a detecção de hifas de Lasiodiplodia theobromae, mesmo quando esses dois fungos estavam num mesmo tecido, como na doença-complexo seca de mangueira investigada no Sultanato de Omã. Além de eucalipto, mangueira (Mangifera indica) e cacaueiro (Theobroma cacao) é provável que essa técnica possa ser estendida para outros hospedeiros lenhosos de C. fimbriata.


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