RESUMO
Publishing research data using a findable, accessible, interoperable, and reusable (FAIR) approach is paramount to further innovation in many areas of research. In particular in developing innovative approaches to predict (eco)toxicological risks in (nano or advanced) material design where efficient use of existing data is essential. The use of tools assessing the FAIRness of data helps the future improvement of data FAIRness and therefore their re-use. This paper reviews ten FAIR assessment tools that have been evaluated and characterized using two datasets from the nanomaterials and microplastics risk assessment domain. The tools were grouped into four categories: online and offline self-assessment survey based, online (semi-) automated and other tools. We found that the online self-assessment tools can be used for a quick scan of a user's dataset due to their ease of use, little need for experience and short time investment. When a user is looking to assess full databases, and not just datasets, for their FAIRness, (semi-)automated tools are more practical. The offline assessment tools were found to be limited and unreliable due to a lack of guidance and an under-developed state. To further characterize the usability, two datasets were run through all tools to check the similarity in the tools' results. As most of the tools differ in their implementation of the FAIR principles, a large variety in outcomes was obtained. Furthermore, it was observed that only one tool gives recommendations to the user on how to improve the FAIRness of the evaluated dataset. This paper gives clear recommendations for both the user and the developer of FAIR assessment tools.
Assuntos
Gerenciamento de Dados , Plásticos , Bases de Dados Factuais , Medição de Risco , Autoavaliação (Psicologia)RESUMO
Five to seven percent of lung tumours are estimated to occur because of occupational asbestos exposure. Using cDNA microarrays, we have earlier detected asbestos exposure-related genomic regions in lung cancer. The region at 2p was one of those that differed most between asbestos-exposed and non-exposed patients. Now, we evaluated genomic alterations at 2p22.1-p16.1 as a possible marker for asbestos exposure. Lung tumours from 205 patients with pulmonary asbestos fibre counts from 0 to 570 million fibres per gram of dry lung, were studied by fluorescence in situ hybridisation (FISH) for DNA copy number alterations (CNA). The prevalence of loss at 2p16, shown by three different FISH probes, was significantly increased in lung tumours of asbestos-exposed patients compared with non-exposed (P=0.05). In addition, a low copy number loss at 2p16 associated significantly with high-level asbestos exposure (P=0.02). Furthermore, 27 of the tumours were studied for allelic imbalances (AI) at 2p22.1-p16.1 using 14 microsatellite markers and also AI at 2p16 was related to asbestos exposure (P=0.003). Our results suggest that alterations at 2p16 combined with other markers could be useful in diagnosing asbestos-related lung cancer.
Assuntos
Desequilíbrio Alélico/genética , Amianto/toxicidade , Cromossomos Humanos Par 2 , DNA de Neoplasias/genética , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Mapeamento Cromossômico , Feminino , Marcadores Genéticos , Humanos , Hibridização in Situ Fluorescente , Neoplasias Pulmonares/patologia , Neoplasias Pulmonares/cirurgia , Masculino , Repetições de Microssatélites/genética , Pessoa de Meia-Idade , Análise de Sequência com Séries de OligonucleotídeosRESUMO
This paper presents a comprehensive review of European Union (EU) legislation addressing the safety of chemical substances, and possibilities within each piece of legislation for applying grouping and read-across approaches for the assessment of nanomaterials (NMs). Hence, this review considers both the overarching regulation of chemical substances under REACH (Regulation (EC) No 1907/2006 on registration, evaluation, authorization, and restriction of chemicals) and CLP (Regulation (EC) No 1272/2008 on classification, labeling and packaging of substances and mixtures) and the sector-specific pieces of legislation for cosmetic, plant protection and biocidal products, and legislation addressing food, novel food, and food contact materials. The relevant supporting documents (e.g. guidance documents) regarding each piece of legislation were identified and reviewed, considering the relevant technical and scientific literature. Prospective regulatory needs for implementing grouping in the assessment of NMs were identified, and the question whether each particular piece of legislation permits the use of grouping and read-across to address information gaps was answered.
Assuntos
Nanoestruturas/classificação , Nanoestruturas/toxicidade , Nanotecnologia/legislação & jurisprudência , Nanotecnologia/métodos , Determinação de Ponto Final , União Europeia , Regulamentação Governamental , Humanos , Estudos Prospectivos , Medição de RiscoRESUMO
Asbestos is a pulmonary carcinogen known to give rise to DNA and chromosomal damage, but the exact carcinogenic mechanisms are still largely unknown. In this study, gene expression arrays were performed on lung tumor samples from 14 heavily asbestos-exposed and 14 non-exposed patients matched for other characteristics. Using a two-step statistical analysis, 47 genes were revealed that could differentiate the tumors of asbestos-exposed from those of non-exposed patients. To identify asbestos-associated regions with DNA copy number and expressional changes, the gene expression data were combined with comparative genomic hybridization microarray data. As a result, a combinatory profile of DNA copy number aberrations and expressional changes significantly associated with asbestos exposure was obtained. Asbestos-related areas were detected in 2p21-p16.3, 3p21.31, 5q35.2-q35.3, 16p13.3, 19p13.3-p13.1 and 22q12.3-q13.1. The most prominent of these, 19p13, was further characterized by microsatellite analysis in 62 patients for the differences in allelic imbalance (AI) between the two groups of lung tumors. 79% of the exposed and 45% of the non-exposed patients (P=0.008) were found to be carriers of AI in their lung tumors. In the exposed group, AI in 19p was prevalent regardless of the histological tumor type. In adenocarcinomas, AI in 19p appeared to occur independently of the asbestos exposure.