Identification of a key protein set involved in Moniliophthora perniciosa necrotrophic mycelium and basidiocarp development.

Moniliophthora perniciosa is a hemibiotrophic fungus that causes witches' broom disease in cacao (Theobroma cacao L.). The biotrophic fungal phase initiates the disease and is characterized by a monokaryotic mycelium, while the necrotrophic phase is characterized by a dikaryotic mycelium and leads to necrosis of infected tissues. A study of the necrotrophic phase was conducted on bran-based solid medium, which is the only medium that enables basidiocarp and basidiospore production. Six different fungal developmental phases were observed according to the mycelium colour or the organ produced: white, yellow, pink, dark pink, primordium and basidiocarp. In this study, we identified notable proteins in each phase, particularly those accumulated prior to basidiocarp formation. Proteins were analysed by proteomics; 2-D gels showed 300-550 spots. Statistically differentially accumulated spots were sequenced by mass spectrometry and 259 proteins were identified and categorized into nine functional classes. Proteins related to energy metabolism, protein folding and morphogenesis that were potentially involved in primordium and basidiocarp formation were identified; these proteins may represent useful candidates for further analysis related to the spread and pathogenesis of this fungus. To the best of our knowledge, this report describes the first proteomic analysis of the developmental phases of Moniliophthora perniciosa.

Impact of vitamin deficiency on microbiota composition and immunomodulation: relevance to autistic spectrum disorders.

OBJECTIVES: Inappropriate vitamin supply is a public health problem and is related to abnormalities in brain development, immune response and, more recently, in changes of gut microbial composition. It is known that low levels of vitamin in early life are linked to increased susceptibility to neurodevelopmental disorders, such as Autism Spectrum Disorders (ASD). Unfortunately, the possible peripheral influences of vitamin deficiency that leads to alterations in the gut microbiota-immune-brain axis, one important modulator of the ASD pathology, remain unclear. This narrative review discusses how the impact of vitamin deficiency results in changes in the immune regulation and in the gut microbiota composition, trying to understand how these changes may contribute for the development and severity of ASD. METHODS: The papers were selected using Pubmed and other databases. This review discusses the following topics: (1) vitamin deficiency in alterations of central nervous system in autism, (2) the impact of low levels of vitamins in immunomodulation and how it can favor imbalance in gut microbiota composition and gastrointestinal (GI) disturbances, (3) gut microbiota imbalance/inflammation associated with the ASD pathophysiology, and (4) possible evidences of the role of vitamin deficiency in dysfunctional gut microbiota-immune-brain axis in ASD. RESULTS: Studies indicate that hypovitaminosis A, B12, D, and K have been co-related with the ASD neuropathology. Furthermore, it was shown that low levels of these vitamins favor the Th1/Th17 environment in the gut, as well as the growth of enteropathogens linked to GI disorders. DISCUSSION: GI disorders and alterations in the gut microbiota-immune-brain axis seems to be linked with ASD severity. Although unclear, hypovitaminosis appears to regulate peripherally the ASD pathophysiology by modulating the gut microbiota-immune-brain axis, however, more research is still necessary to confirm this hypothesis.

Copper and Neurotoxicity in Autism Spectrum Disorder.

Free radicals (FR) act on living organisms and present unpaired electrons in the molecular orbitals of oxygen or nitrogen species. They are classified as redox reactions and account for a wide range of processes in biological systems. Genetic and environmental factors may alter the levels of FR in the cell, leading to deleterious consequences such as membrane lipid peroxidation, protein nitration, enzyme, carbohydrate and DNA damage, ultimately resulting in premature aging and a pro-inflammatory microenvironment as observed in Alzheimer's disease (AD) and autism spectrum disorder (ASD). O2 radical ability to act as a Lewis base and to form a complex with metal transition such as iron and copper (Lewis acids) leads to biomolecules oxidation at physiological pH, thus increasing the possibility of injury and oxidative damage in biological tissues. In this review, we discuss the role of metals, like copper, and the amyloid precursor protein (APP) derivative (s-APP-alpha) as an antioxidant and a possible adjuvant in the treatment of some autistic spectrum disorder symptoms (ASD).

Avaliação do limiar sensorial para gosto doce no autismo infantil / Sensory threshold evaluation for sweet taste in childhood autism

Objetivo: avaliar a sensibilidade gustativa ao doce de crianças com Transtorno do Espectro Autista. Método: trata-se de estudo quantitativo, descritivo e transversal, com crianças diagnosticadas e sem diagnóstico com Transtorno e familiares. Avaliou-se o grau de autismo por meio da Childhood Autism Rating Scale para selecionar crianças com nível de autismo compatível com a realização dos testes. Executou-se o teste de índice limiar de boca toda para o gosto doce com diferentes concentrações de sacarose em todos os grupos. Realizou-se o teste de preferência sensorial no grupo de crianças com TEA. Executaram-se as análises no Statistical Package for the Social Sciences. Resultados: observou-se que as crianças sem Transtorno apresentam limiar gustativo médio para o gosto doce de 0,96 g/L de sacarose, limiar inferior ao de crianças com TEA (5,42 g/L de sacarose); as mães e irmãos das crianças com Transtorno apresentaram limiar gustativo médio de 1,23 g/L e 1,35g/L de sacarose, respectivamente. Averiguou-se, no teste de preferência sensorial, que crianças com Transtorno preferem amostras com gostos mais doces. Conclusão: percebeu-se que crianças com Transtorno possuem alteração na sensibilidade gustativa para o doce, necessitando de maiores quantidades de sacarose para identificar este gosto.(AU)

Objective: to evaluate the sweet taste sensitivity of children with Autistic Spectrum Disorder. Method: this is a quantitative, descriptive and cross-sectional study with children diagnosed and undiagnosed with the disorder and their families. The degree of autism was assessed using the Childhood Autism Rating Scale to select children with level of autism compatible with the tests. The whole mouth threshold index test for sweet taste with different sucrose concentrations was performed in all groups. The sensory preference test was performed in the group of children with ASD. Analyzes were performed on the Statistical Package for the Social Sciences. Results: it was observed that children without Disorder presented an average sweet taste threshold of 0.96 g / L sucrose, lower threshold than children with ASD (5.42 g / L sucrose); mothers and siblings of children with the disorder had a mean taste threshold of 1.23 g / l and 1.35 g / l of sucrose, respectively. In the sensory preference test, children with disorder prefer samples with sweeter tastes. Conclusion: it was noticed that children with Disorder have alterations in taste sensitivity for sweets, requiring higher amounts of sucrose to identify this taste.(AU)

Objetivo: evaluar la sensibilidad al sabor dulce de los niños con Trastorno del Espectro Autista. Método: se trata de un estudio cuantitativo, descriptivo y transversal con niños diagnosticados y no diagnosticados con el Trastorno y sus familias. El grado de autismo se evaluó utilizando la Escala de Calificación de Autismo Infantil para seleccionar niños con un nivel de autismo compatible con las pruebas. La prueba de índice de umbral de boca completa para el sabor dulce con diferentes concentraciones de sacarosa se realizó en todos los grupos. La prueba de preferencia sensorial se realizó en el grupo de niños con TEA. Se realizaron análisis en el Paquete Estadístico para las Ciencias Sociales. Resultados: se observó que los niños sin Trastorno presentaron un umbral promedio de sabor dulce de 0.96 g/l de sacarosa, umbral más bajo que los niños con TEA (5.42 g/l de sacarosa); las madres y los hermanos de niños con el Trastorno tenían un umbral de sabor medio de 1,23 g/l y 1,35 g/l de sacarosa, respectivamente. En la prueba de preferencia sensorial, los niños con Trastorno prefieren muestras con sabores más dulces. Conclusión: se notó que los niños con Trastorno tienen alteraciones en la sensibilidad al sabor de los dulces, lo que requiere mayores cantidades de sacarosa para identificar este sabor.(AU)

SUR1 Receptor Interaction with Hesperidin and Linarin Predicts Possible Mechanisms of Action of Valeriana officinalis in Parkinson.

Parkinson's disease (PD) is one of the most common neurodegenerative disorders. A theoretical approach of our previous experiments reporting the cytoprotective effects of the Valeriana officinalis compounds extract for PD is suggested. In addiction to considering the PD as a result of mitochondrial metabolic imbalance and oxidative stress, such as in our previous in vitro model of rotenone, in the present manuscript we added a genomic approach to evaluate the possible underlying mechanisms of the effect of the plant extract. Microarray of substantia nigra (SN) genome obtained from Allen Brain Institute was analyzed using gene set enrichment analysis to build a network of hub genes implicated in PD. Proteins transcribed from hub genes and their ligands selected by search ensemble approach algorithm were subjected to molecular docking studies, as well as 20 ns Molecular Dynamics (MD) using a Molecular Mechanic Poison/Boltzman Surface Area (MMPBSA) protocol. Our results bring a new approach to Valeriana officinalis extract, and suggest that hesperidin, and probably linarin are able to relieve effects of oxidative stress during ATP depletion due to its ability to binding SUR1. In addition, the key role of valerenic acid and apigenin is possibly related to prevent cortical hyperexcitation by inducing neuronal cells from SN to release GABA on brain stem. Thus, under hyperexcitability, oxidative stress, asphyxia and/or ATP depletion, Valeriana officinalis may trigger different mechanisms to provide neuronal cell protection.