EVALITA 2020: Overview of the 7th evaluation campaign of natural language processing and speech tools for Italian

The Evaluation Campaign of Natural Language Processing and Speech Tools for Italian (EVALITA) is the biennial initiative aimed at promoting the development of language and speech technologies for the Italian language. EVALITA is promoted by the Italian Association of Computational Linguistics (AILC) and it is endorsed by the Italian Association for Artificial Intelligence (AIxIA) and the Italian Association for Speech Sciences (AISV). EVALITA provides a shared framework where different systems and approaches can be scientifically evaluated and compared with each other with respect to a large variety of tasks, suggested and organized by the Italian research community. The proposed tasks represent scientific challenges where methods, resources, and systems can be tested against shared benchmarks representing linguistic open issues or real world applications, possibly in a multilingual and/or multi-modal perspective. The collected data sets provide big opportunities for scientists to explore old and new problems concerning NLP in Italian as well as to develop solutions and to discuss the NLP-related issues within the community. Some tasks are traditionally present in the evaluation campaign, while others are completely new. This paper introduces the tasks proposed at EVALITA 2020 and provides an overview to the participants and systems whose descriptions and obtained results are reported in these Proceedings

Spectrofluorometric analysis of autofluorescing components of crude serum from a rat liver model of ischemia and reperfusion

Autofluorescence (AF) of crude serum was investigated with reference to the potential of its intrinsic AF biomarkers for the noninvasive diagnosis of liver injury. Spectral parameters of pure compounds representing retinol (vitamin A) and fluorescing free fatty acids were characterized by spectrofluorometry, to assess spectral parameters for the subsequent AF analysis of serum, collected from rats undergoing liver ischemia/reperfusion (I/R). Differences in AF spectral profiles detected between control and I/R were due to the increase in the AF components representing fatty acids in I/R serum samples. No significant changes occurred for retinol levels, consistently with the literature reporting that constant retinol levels are commonly observed in the blood, except for malnutrition or chronic severe liver disease. Conversely, fatty acids, in particular arachidonic and linoleic acid and their derivatives, act as modulating agents in inflammation, representing both a protective and damaging response to stress stimuli. The biometabolic and pathophysiological meaning of serum components and the possibility of their direct detection by AF spectrofluorometry open up interesting perspectives for the development of AF serum analysis, as a direct, cost effective, supportive tool to assess liver injury and related systemic metabolic alterations, for applications in experimental biomedicine and foreseen translation to the clinics

Medical reporting recommendations: a gap between practical and theoretical approach of journalists in Italy

This survey involved medical reporters to identify degrees of theoretical and actual com\uacpliance to recommendations for health reporting. Methods The questionnaire was addressed to 450 Italian journalists and obtained a redemption of 23.1%. Major gaps between theoretical agreement and professional practice were: need of scientific background and continuing education; importance of avoiding sensationalism, assessment of scientific protocols and results, reporting of results as abso\uaclute risk and numbers needed to treat, attention to the conflict of interest. Two homogeneous pro\uacfiles emerged. Group 1 includes journalists working in newspapers and shows a large gap between theory and practice. Group 2 includes mainly journalists working in technical medical media and shows a higher consistency between the two settings. An improvement in theoretical understanding of medical literature is advisable, but interventions are needed in the working practice in particular in newspapers, a setting where approaches are more difficult

Microenvironment in neuroblastoma: Isolation and characterization of tumor-derived mesenchymal stromal cells

Background: It has been proposed that mesenchymal stromal cells (MSCs) promote tumor progression by interacting with tumor cells and other stroma cells in the complex network of the tumor microenvironment. We characterized MSCs isolated and expanded from tumor tissues of pediatric patients diagnosed with neuroblastomas (NB-MSCs) to define interactions with the tumor microenvironment. Methods: Specimens were obtained from 7 pediatric patients diagnosed with neuroblastoma (NB). Morphology, immunophenotype, differentiation capacity, proliferative growth, expression of stemness and neural differentiation markers were evaluated. Moreover, the ability of cells to modulate the immune response, i.e. inhibition of phytohemagglutinin (PHA) activated peripheral blood mononuclear cells (PBMCs) and natural killer (NK) cytotoxic function, was examined. Gene expression profiles, known to be related to tumor cell stemness, Wnt pathway activation, epithelial-mesenchymal transition (EMT) and tumor metastasis were also evaluated. Healthy donor bone marrow-derived MSCs (BM-MSC) were employed as controls. Results: NB-MSCs presented the typical MSC morphology and phenotype. They showed a proliferative capacity superimposable to BM-MSCs. Stemness marker expression (Sox2, Nanog, Oct3/4) was comparable to BM-MSCs. NB-MSC in vitro osteogenic and chondrogenic differentiation was similar to BM-MSCs, but NB-MSCs lacked adipogenic differentiation capacity. NB-MSCs reached senescence phases at a median passage of P7 (range, P5-P13). NB-MSCs exhibited greater immunosuppressive capacity on activated T lymphocytes at a 1:2 (MSC: PBMC) ratio compared with BM-MSCs (p = 0.018). NK cytotoxic activity was not influenced by co-culture, either with BM-MSCs or NB-MSCs. Flow-cytometry cell cycle analysis showed that NB-MSCs had an increased number of cells in the G0-G1 phase compared to BM-MSCs. Transcriptomic profiling results indicated that NB-MSCs were enriched with EMT genes compared to BM-MSCs. Conclusions: We characterized the biological features, the immunomodulatory capacity and the gene expression profile of NB-MSCs. The NB-MSC gene expression profile and their functional properties suggest a potential role in promoting tumor escape, invasiveness and metastatic traits of NB cancer cells. A better understanding of the complex mechanisms underlying the interactions between NB cells and NB-derived MSCs should shed new light on potential novel therapeutic approaches

Repression of Esophageal Neoplasia and Inflammatory Signaling by Anti-miR-31 Delivery In Vivo.

BACKGROUND: Overexpression of microRNA-31 (miR-31) is implicated in the pathogenesis of esophageal squamous cell carcinoma (ESCC), a deadly disease associated with dietary zinc deficiency. Using a rat model that recapitulates features of human ESCC, the mechanism whereby Zn regulates miR-31 expression to promote ESCC is examined. METHODS: To inhibit in vivo esophageal miR-31 overexpression in Zn-deficient rats (n = 12-20 per group), locked nucleic acid-modified anti-miR-31 oligonucleotides were administered over five weeks. miR-31 expression was determined by northern blotting, quantitative polymerase chain reaction, and in situ hybridization. Physiological miR-31 targets were identified by microarray analysis and verified by luciferase reporter assay. Cellular proliferation, apoptosis, and expression of inflammation genes were determined by immunoblotting, caspase assays, and immunohistochemistry. The miR-31 promoter in Zn-deficient esophagus was identified by ChIP-seq using an antibody for histone mark H3K4me3. Data were analyzed with t test and analysis of variance. All statistical tests were two-sided. RESULTS: In vivo, anti-miR-31 reduced miR-31 overexpression (P = .002) and suppressed the esophageal preneoplasia in Zn-deficient rats. At the same time, the miR-31 target Stk40 was derepressed, thereby inhibiting the STK40-NF-κΒ-controlled inflammatory pathway, with resultant decreased cellular proliferation and activated apoptosis (caspase 3/7 activities, fold change = 10.7, P = .005). This same connection between miR-31 overexpression and STK40/NF-κΒ expression was also documented in human ESCC cell lines. In Zn-deficient esophagus, the miR-31 promoter region and NF-κΒ binding site were activated. Zn replenishment restored the regulation of this genomic region and a normal esophageal phenotype. CONCLUSIONS: The data define the in vivo signaling pathway underlying interaction of Zn deficiency and miR-31 overexpression in esophageal neoplasia and provide a mechanistic rationale for miR-31 as a therapeutic target for ESCC

Trans-generational epigenetic regulation associated with the amelioration of Duchenne Muscular Dystrophy

Exon skipping is an effective strategy for the treatment of many Duchenne Muscular Dystrophy (DMD) mutations. Natural exon skipping observed in several DMD cases can help in identifying novel therapeutic tools. Here, we show a DMD study case where the lack of a splicing factor (Celf2a), which results in exon skipping and dystrophin rescue, is due to a maternally inherited trans-generational epigenetic silencing. We found that the study case and his mother express a repressive long non-coding RNA, DUXAP8, whose presence correlates with silencing of the Celf2a coding region. We also demonstrate that DUXAP8 expression is lost upon cell reprogramming and that, upon induction of iPSCs into myoblasts, Celf2a expression is recovered leading to the loss of exon skipping and loss of dystrophin synthesis. Finally, CRISPR/Cas9 inactivation of the splicing factor Celf2a was proven to ameliorate the pathological state in other DMD backgrounds establishing Celf2a ablation or inactivation as a novel therapeutic approach for the treatment of Duchenne Muscular Dystrophy

Relevant but neglected habitat types by the Directive 92/43 EEC in southern Italy

The 92/43/EEC Habitats Directive is the main European Union legal tool concerning nature conservation. The habitat types listed in Annex I to the Directive are phytosociology-based. It is widely acknowledged that phytosociological analysis is a crucial approach for habitats characterization and for monitoring their conservation status. Based on bibliographic investigations and new field survey campaigns, a list of habitat types neglected by the Habitats Directive is here presented and described for southern Italy. In this paper, 8 new habitat types and 13 subtypes are proposed. For each of these proposed new habitat types, a wide range of information, including ecology, chorology, species composition, syntaxonomy, threats, and conservation status, is here provided. To supply more detailed phytogeographical and coenological information about the proposed new habitat types, distribution maps based on 10 x 10 km reference grids and phytosociological tables including unpublished releves were carried out

Genome-wide activity of unliganded estrogen receptor-\u3b1\ua0 in breast cancer cells

Estrogen receptor-\u3b1 (ER\u3b1) has central role in hormone-dependent breast cancer and its ligand-induced functions have been extensively characterized. However, evidence exists that ER\u3b1 has functions that are independent of ligands. In the present work, we investigated the binding of ER\u3b1 to chromatin in the absence of ligands and its functions on gene regulation. We demonstrated that in MCF7 breast cancer cells unliganded ER\u3b1 binds to more than 4,000 chromatin sites. Unexpectedly, although almost entirely comprised in the larger group of estrogen-induced binding sites, we found that unliganded-ER\u3b1 binding is specifically linked to genes with developmental functions, compared with estrogen-induced binding. Moreover, we found that siRNA-mediated down-regulation of ER\u3b1 in absence of estrogen is accompanied by changes in the expression levels of hundreds of coding and noncoding RNAs. Down-regulatedmRNAs showed enrichment in genes related to epithelial cell growth and development. Stable ER\u3b1 down-regulation using shRNA, which caused cell growth arrest, was accompanied by increased H3K27me3 at ER\u3b1 binding sites. Finally, we found that FOXA1 and AP2\u3b3 binding to several sites is decreased upon ER\u3b1 silencing, suggesting that unliganded ER\u3b1 participates, together with other factors, in the maintenance of the luminal-specific cistrome in breast cancer cell

Genome-wide association study provides insights into genes related with horn development in Nelore beef cattle.

Abstract The causal mutation for polledness in Nelore (Bos taurus indicus) breed seems to have appeared first in Brazil in 1957. The expression of the polled trait is known to be ruled by a few groups of alleles in taurine breeds; however, the genetic basis of this trait in indicine cattle is still unclear. The aim of this study was to identify genomic regions associated with the hornless trait in a commercial Nelore population. A total of 107,294 animals had phenotypes recorded and 2,238 were genotyped/imputed for 777k SNP. The weighted single-step approach for genome-wide association study (WssGWAS) was used to estimate the SNP effects and variances accounted for by 1 Mb sliding SNP windows. A centromeric region of chromosome 1 with 3.11 Mb size (BTA1: 878,631?3,987,104 bp) was found to be associated with hornless in the studied population. A total of 28 protein-coding genes are mapped in this region, including the taurine Polled locus and the IFNAR1, IFNAR2, IFNGR2, KRTAP11-1, MIS18A, OLIG1, OLIG2, and SOD1 genes, which expression can be related to the horn formation as described in literature. The functional enrichment analysis by DAVID tool revealed cytokine-cytokine receptor interaction, JAK-STAT signaling, natural killer cell mediated cytotoxicity, and osteoclast differentiation pathways as significant (P < 0.05). In addition, a runs of homozygosity (ROH) analysis identified a ROH island in polled animals with 2.47 Mb inside the region identified by WssGWAS. Polledness in Nelore cattle is associated with one region in the genome with 3.1 Mb size in chromosome 1. Several genes are harbored in this region, and they may act together in the determination of the polled/horned phenotype. Fine mapping the locus responsible for polled trait in Nelore breed and the identification of the molecular mechanisms regulating the horn growth deserve further investigation