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This article provides a systematic review of research conducted on the proteomic composition of blood as part of a complex biological age estimation. We performed a comprehensive analysis of 17 publicly available datasets and compiled an integral list of proteins. These proteins were sorted based on their detection probability using mass spectrometry in human plasma. We propose this list as a basis for creating a panel of peptides and quantifying the content of selected proteins in the format of a proteomic aging clock. The selected proteins are especially notable for their roles in inflammatory processes and lipid metabolism. Our findings suggest, for the first time, that proteins associated with systemic disorders, including those approved by the FDA for clinical use, could serve as potential markers of aging. [ABSTRACT FROM AUTHOR]

Recently, cerebral folate deficiency (CFD) was suggested to be involved in the pathogenesis of autism spectrum disorders (ASD). However, the exact role of folate metabolism in the pathogenesis of ASD, identification of underlying pathogenic mechanisms and impaired metabolic pathways remain unexplained. The aim of our study was to develop and test a novel, unbiased, bioinformatics approach in order to identify links between ASD and disturbed cerebral metabolism by focusing on abnormal folate metabolism, which could foster patient stratification and novel therapeutic interventions. An unbiased, automatable, computational workflow interaction model was developed using available data from public databases. The interaction network model of ASD-associated genes with known cerebral expression and function (SFARI) and metabolic networks (MetScape), including connections to known metabolic substrates, metabolites and cofactors involving folates, was established. Intersection of bioinformatically created networks resulted in a limited amount of interaction modules pointing to common disturbed metabolic pathways, linking ASD to CFD. Two independent interaction modules (comprising three pathways) covering enzymes encoded by ASD-related genes and folate cofactors utilizing enzymes were generated. Module 1 suggested possible interference of CFD with serine and lysine metabolism, while module 2 identified correlations with purine metabolism and inosine monophosphate production. Since our approach was primarily conceived as a proof of principle, further amendments of the presented initial model are necessary to obtain additional actionable outcomes. Our modelling strategy identified not only previously known interactions supported by evidence-based analyses, but also novel plausible interactions, which could be validated in subsequent functional and/or clinical studies. Autism Res 2017, 10: 1424-1435. © 2017 International Society for Autism Research, Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Surveillance and traceability of medical devices (MD) is a challenge in health care systems. In the perspective of reusing EHR data to automate the monitoring of medical devices, we carried out a comparison of the main MD knowledge bases (MD-KDB) currently available in France. Four MD-KDBs (ANSM, Gudid, Exhausmed and CIOdm) were compared quantitatively and through an example of a shoulder prosthesis. The number of MDs registered differs from one MD-KDB to another. Domain terminologies used in MD-KDBs differ in terms of granularity and in the ease of querying. Waiting EUDAMED, the European MD-KDB, it seems necessary so far to use and combine information coming from several MD-KDBs to address MD monitoring. [ABSTRACT FROM AUTHOR]

The analysis of temporal changes in the number of scientific articles written on ecosystem services shows an exponential growth from 1991 to 2013. However, it also shows a lack of information regarding the location of the studies and the type of ecosystem analyzed. A literature search showed that some regions (Antarctica) and ecosystems (urban) have been less studied. However, given the structure of the knowledge databases it is impossible to know if there are no studies or it is difficult to reach them. [ABSTRACT FROM AUTHOR]

Recently, cerebral folate deficiency (CFD) was suggested to be involved in the pathogenesis of autism spectrum disorders (ASD). However, the exact role of folate metabolism in the pathogenesis of ASD, identification of underlying pathogenic mechanisms and impaired metabolic pathways remain unexplained. The aim of our study was to develop and test a novel, unbiased, bioinformatics approach in order to identify links between ASD and disturbed cerebral metabolism by focusing on abnormal folate metabolism, which could foster patient stratification and novel therapeutic interventions. An unbiased, automatable, computational workflow interaction model was developed using available data from public databases. The interaction network model of ASD-associated genes with known cerebral expression and function (SFARI) and metabolic networks (MetScape), including connections to known metabolic substrates, metabolites and cofactors involving folates, was established. Intersection of bioinformatically created networks resulted in a limited amount of interaction modules pointing to common disturbed metabolic pathways, linking ASD to CFD. Two independent interaction modules (comprising three pathways) covering enzymes encoded by ASD-related genes and folate cofactors utilizing enzymes were generated. Module 1 suggested possible interference of CFD with serine and lysine metabolism, while module 2 identified correlations with purine metabolism and inosine monophosphate production. Since our approach was primarily conceived as a proof of principle, further amendments of the presented initial model are necessary to obtain additional actionable outcomes. Our modelling strategy identified not only previously known interactions supported by evidence-based analyses, but also novel plausible interactions, which could be validated in subsequent functional and/or clinical studies. Autism Res 2017, 10: 1424-1435. © 2017 International Society for Autism Research, Wiley Periodicals, Inc., (© 2017 International Society for Autism Research, Wiley Periodicals, Inc.)