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

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). 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Motor System Changes in the Aging Brain: What is Normal and What is Not

Age-related changes in the nervous system may present with physical signs that are not unlike early manifestations of several clinical disorders. Gait disturbances (immobility), balance difficulties (instability), and certain motor control problems (i.e., tremor) are not necessarily signs of a disease state. The clinician needs to be reminded that most physiologic functions decline at a rate of 1% per year, beginning at age 30. Often compounding natural decline are the motor problems related to disuse. This is especially true for the inactive individual suffering from depression, cardiac or pulmonary insufficiency, painful joint and muscle conditions, substance abuse and, sometimes, simply social isolatio

Abraham Lincoln May Have Had SCA Type 5

In his recent Historical Neurology article, Dr. Sotos concludes that it is highly unlikely that President Lincoln inherited the gene for SCA5. The author asserts that there is a lack of evidence indicating that the gene entered the Lincoln pedigree prior to generation V. In addition, the author notes that handwriting samples and historical anecdotes can be used to draw the conclusion that neither President Lincoln nor his grandmother Bathsheba Herring had SCA5. We disagre

Spectrin Mutations Cause Spinocerebellar Ataxia Type 5

We have discovered that beta-III spectrin (SPTBN2) mutations cause spinocerebellar ataxia type 5 (SCA5) in an 11-generation American kindred descended from President Lincoln\u27s grandparents and two additional families. Two families have separate in-frame deletions of 39 and 15 bp, and a third family has a mutation in the actin/ARP1 binding region. Beta-III spectrin is highly expressed in Purkinje cells and has been shown to stabilize the glutamate transporter EAAT4 at the surface of the plasma membrane. We found marked differences in EAAT4 and GluRdelta2 by protein blot and cell fractionation in SCA5 autopsy tissue. Cell culture studies demonstrate that wild-type but not mutant beta-III spectrin stabilizes EAAT4 at the plasma membrane. Spectrin mutations are a previously unknown cause of ataxia and neurodegenerative disease that affect membrane proteins involved in glutamate signaling

Spinocerebellar Ataxia Type 8: Clinical Features in a Large Family

OBJECTIVE: To compare the clinical and genetic features of the seven-generation family (MN-A) used to define the spinocerebellar ataxia 8 (SCA8) locus. BACKGROUND: The authors recently described an untranslated CTG expansion that causes a novel form of SCA (SCA8) characterized by reduced penetrance and complex patterns of repeat instability. METHODS: Clinical and molecular features of 82 members of the MN-A family were evaluated by neurologic examination, quantitative dexterity testing, and, in some individuals, MRI and sperm analyses. RESULTS: SCA8 is a slowly progressive, predominantly cerebellar ataxia with marked cerebellar atrophy, affecting gait, swallowing, speech, and limb and eye movements. CTG tracts are longer in affected (mean = 116 CTG repeats) than in unaffected expansion carriers (mean = 90, p \u3c 10-8). Quantitative dexterity testing did not detect even subtle signs of ataxia in unaffected expansion carriers. Surprisingly, all 21 affected MN-A family members inherited an expansion from their mothers. The maternal penetrance bias is consistent with maternal repeat expansions yielding alleles above the pathogenic threshold in the family (\u3e107 CTG) and paternal contractions resulting in shorter alleles. Consistent with the reduced penetrance of paternal transmissions, CTG tracts in all or nearly all sperm (84 to 99) are significantly shorter than in the blood (116) of an affected man. CONCLUSIONS: The biologic relationship between repeat length and ataxia indicates that the CTG repeat is directly involved in SCA8 pathogenesis. Diagnostic testing and genetic counseling are complicated by the reduced penetrance, which often makes the inheritance appear recessive or sporadic, and by interfamilial differences in the length of a stable (CTA)n tract preceding the CTG repeat

Immunoreactive levels of α-ketoglutarate dehydrogenase subunits in Friedreich's ataxia and spinocerebellar ataxia type 1

peer reviewe

Lobe-specific increases in malondialdehyde DNA adduct formation in the livers of mice following infection with Helicobacter hepaticus

Helicobacter hepaticus infection is associated with chronic hepatitis and the development of liver tumours in mice. The underlying mechanism of this liver carcinogenesis is not clear but the oxidative stress associated with H. hepaticus infection may result in induction of lipid peroxidation and the generation of malondialdehyde. Malondialdehyde can react with deoxyguanosine in DNA resulting in the formation of the cyclic pyrimidopurinone N-1,N-2 malondialdehyde-deoxyguanosine (M(1)dG) adduct. This adduct has the potential to cause mutations that may ultimately lead to liver carcinogenesis. The objective of this study was to determine the control and infection-related levels of M(1)dG in the liver DNA of mice over time, using an immunoslot-blot procedure. The level of M(1)dG in control A/J mouse livers at 3, 6, 9 and 12 months averaged 37.5, 36.6, 24.8 and 30.1 adducts per 10(8) nucleotides, respectively. Higher levels of M(1)dG were detected in the liver DNA of H. hepaticus infected A/JCr mice, with levels averaging 40.7, 47.0, 42.5 and 52.5 adducts per 10(8) nucleotides at 3, 6, 9 and 12 months, respectively. There was a significant age dependent increase in the level of M(1)dG in the caudate and median lobes of the A/JCr mice relative to control mice. A lobe specific distribution of the M(1)dG adduct in both infected and control mice was noted, with the left lobe showing the lowest level of the adduct compared with the right and median lobes at all time points. In a separate series of mice experimentally infected with H. hepaticus, levels of 8-hydroxy-deoxyguanosine were significantly greater in the median compared with the left lobe at 12 weeks after treatment. In conclusion, these results suggest that M(1)dG occurs as a result of oxidative stress associated with H. hepaticus infection of mice, and may contribute to liver carcinogenesis in this model