Assessment of the Effect of Satureja montana and Origanum virens Essential Oils on Aspergillus flavus Growth and Aflatoxin Production at Different Water Activities

© 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).Aflatoxin contamination of foodstuffs poses a serious risk to food security, and it is essential to search for new control methods to prevent these toxins entering the food chain. Several essential oils are able to reduce the growth and mycotoxin biosynthesis of toxigenic species, although their efficiency is strongly influenced by the environmental conditions. In this work, the effectiveness of Satureja montana and Origanum virens essential oils to control Aspergillus flavus growth was evaluated under three water activity levels (0.94, 0.96 and 0.98 aw) using a Bioscreen C, a rapid in vitro spectrophotometric technique. The aflatoxin concentrations at all conditions tested were determined by HPLC-FLD. Aspergillus flavus growth was delayed by both essential oil treatments. However, only S. montana essential oil was able to significantly affect aflatoxin production, although the inhibition percentages widely differed among water activities. The most significant reduction was observed at 0.96 aw, which is coincident with the conditions in which A. flavus reached the highest levels of aflatoxin production. On the contrary, the treatment with S. montana essential oil was not effective in significantly reducing aflatoxin production at 0.94 aw. Therefore, it is important to study the interaction of the new control compounds with environmental factors before their application in food matrices, and in vitro ecophysiological studies are a good option since they provide accurate and rapid results.Peer reviewedFinal Published versio

Prognostic stratification of adult primary glioblastoma multiforme patients based on their tumor gene amplification profiles

Several classification systems have been proposed to address genomic heterogeneity of glioblastoma multiforme, but they either showed limited prognostic value and/or are difficult to implement in routine diagnostics. Here we propose a prognostic stratification model for these primary tumors based on tumor gene amplification profiles, that might be easily implemented in routine diagnostics, and potentially improve the patients management. Gene amplification profiles were prospectively evaluated in 80 primary glioblastoma multiforme tumors using singlenucleotide polymorphism arrays and the results obtained validated in publicly available data from 267/347 cases. Gene amplification was detected in 45% of pati

Frequently amplified chromosomal regions in GBM.

<p>Detailed characterization of the extension and the gene coded in those segments of chromosomes 1 (A), 4 (B), 7 (C) and 12 (D) found to be recurrently amplified in GBM by SNP-arrays. The identification code for each tumor isplaced on top of each line (G–N.), the length size of the amplicon in Kb is placed at the bottom of the amplified regions, and both the starting and ending positions of the amplicons are shown at the left of each chromosomal region. All genes affected in common for each amplified chromosomal segment are displayed; previously reported candidate genes amplified in a significant number of cases are shown in red, other frequently amplified genes are depicted in blue, whereas genes depicted in black correspond to genes amplified at low frequencies. A total of 6 amplified genes (<i>DCUN1D4, LRRC66*, SGCB, SPATA18, USP46, RASL11B</i>) and fifteen amplicons (<i>LOC644145*, EXOC1, CEP135, KIAA1211, AASDH, PPAT, PAICS, SRP72, ARL9, GLDCP1*, HOPX, REST, C4orf14, POLR2B, IGFBP7</i>) were additionally found in cases G12 and G73, respectively. Genes without expression values in the GEP-array are highlighted with square boxes in the figure and with an asterisk in this legend.</p

Overall survival curves of GBM patients (n = 45) according to the presence vs absence of amplification of the <i>PDGFRA</i> (Panel A), EGFR (Panel B) and <i>MDM4</i> genes (Panel C) and the presence vs absence of deletion of the <i>PTEN</i> gene (Panel D).

<p>Overall survival curves of GBM patients (n = 45) according to the presence vs absence of amplification of the <i>PDGFRA</i> (Panel A), EGFR (Panel B) and <i>MDM4</i> genes (Panel C) and the presence vs absence of deletion of the <i>PTEN</i> gene (Panel D).</p

Clinical characteristics of GBM patients (n = 46) included in this study with information about the type of SNP-arrays used in each case to investigate DNA CN alterations.

<p>Surgical removal: ST- subtotal; T- total.</p>*<p>Tumors analyzed by gene expression arrays.</p>#<p>Only patient that remained alive at the moment of closing the study; all other patients had died.</p

Frequently homozygously deleted chromosomal regions in GBM.

<p>Recurrent homozygously deleted segments of chromosomes 9 (9p21.2 and 9p21.3) (A) and 10 (10p13, 10q11, 10q21, 10q22, 10q23, 10q24 and 10q26) (B). The identification code for each tumor is placed on top of each line (G–N.), the length of the deleted chromosomal region in Kb is placed at the bottom of the lines corresponding to each deleted region, and both the starting and ending positions of the deleted segments are shown at the left of each chromosomal region. All genes coded in each deleted chromosomal region are displayed: previously reported candidate genes deleted in a significant number of cases are shown in red, other recurrently deleted genes are depicted in blue, while genes deleted at low frequencies are shown in black.. Genes without expression values in the array are highlighted with square boxes in the figure.</p

X chromosome inactivation does not necessarily determine the severity of the phenotype in Rett syndrome patients

WOS: 000481590200024PubMed ID: 31427717Rett syndrome (RTT) is a severe neurological disorder usually caused by mutations in the MECP2 gene. Since the MECP2 gene is located on the X chromosome, X chromosome inactivation (XCI) could play a role in the wide range of phenotypic variation of RTT patients; however, classical methylation-based protocols to evaluate XCI could not determine whether the preferentially inactivated X chromosome carried the mutant or the wild-type allele. Therefore, we developed an allele-specific methylation-based assay to evaluate methylation at the loci of several recurrent MECP2 mutations. We analyzed the XCI patterns in the blood of 174 RTT patients, but we did not find a clear correlation between XCI and the clinical presentation. We also compared XCI in blood and brain cortex samples of two patients and found differences between XCI patterns in these tissues. However, RTT mainly being a neurological disease complicates the establishment of a correlation between the XCI in blood and the clinical presentation of the patients. Furthermore, we analyzed MECP2 transcript levels and found differences from the expected levels according to XCI. Many factors other than XCI could affect the RTT phenotype, which in combination could influence the clinical presentation of RTT patients to a greater extent than slight variations in the XCI pattern.Spanish Ministry of Health (Instituto de Salud Carlos III/FEDER) [PI15/01159]; Crowdfunding program PRECIPITA, from the Spanish Ministry of Health (Fundacion Espanola para la Ciencia y la Tecnologia); Catalan Association for Rett Syndrome; Fondobiorett; Mi Princesa RettWe thank all patients and their families who contributed to this study. The work was supported by grants from the Spanish Ministry of Health (Instituto de Salud Carlos III/FEDER, PI15/01159); Crowdfunding program PRECIPITA, from the Spanish Ministry of Health (Fundacion Espanola para la Ciencia y la Tecnologia); the Catalan Association for Rett Syndrome; Fondobiorett and Mi Princesa Rett