529 research outputs found

    SYSTEM-LEVEL HYBRID FAULT DIAGNOSABILITY WITH GENERAL TEST INVALIDATION

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    On the basis of a self-checking system model with general test invalidation the problem of diagnosability in the case of permanent and intermittent faults known as hybrid fault situation is discussed. Two hybrid fault models have been introduced that take into consideration the behaviour of the faulty tester. On the basis of the relationship that exists between the permanent and hybrid fault models, given the number of all units in a system, the upper bound of the number of diagnosable faulty units is defined without restriction on the test connection assignment

    Local risk proneness in analytically approximated utility functions under monotonically decreasing preferences

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    We discuss an analytical arctan form to approximate decreasing utilitiesbased on several nodes of its graphics elicited in interval form. We demonstratethe process on two types of nodes originating from different subjective elicitation approaches. Our focus is also on the local risk attitude estimator, whichin the case of decreasing preferences gets interpreted as local risk proneness vsthe local risk aversion for increasing preferences

    Estimation of errors in text and data processing

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    The company Adiss Lab Lts. obtained 1 000 000 medical reports that are either in free form text, or in XML format. One of the main goals of their development is to integrate an algorithm for information extraction (IE) in their platform. The verification of the algorithm’s output for a report is done by a medical doctor (MD) for a certain fee. Validating the correctness of all data would be overwhelming and very expensive. Hence, the problem, as presented by the company, is to provide a method (algorithm) which determines the minimum amount of reports that will validate the correctness of the IE algorithm and a procedure for selecting these reports. In order to solve the problem we have considered an algorithm-centric approach uses active learning and semi-supervised learning

    NGF-ome: its metabotrophic expression. Homage to Rita Levi-Montalcini

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    Nowadays, in the postgenome time, many "-ome" studies have emerged including proteome, transcriptome, interactome, metabolome, adipokinome, connectome. In this vein, the catchall term NGF-ome embodies all the actions of NGF in health and disease. Accordingly, the present Festschrift, also tabula gratulatoria, is to honor and acknowledge the contributions of the distinguished neuroscientist and magistra Rita Levi-Montalcini, the Nobel Prize winner-1986 for the discoverer of NGF. Today, NGF and another neurotrophin, brain-derived neuroptrophic factor (BDNF), are well recognized to mediate multiple biological phenomena, ranging from the neurotrophic through immunotrophic and epitheliotrophic to metabotrophic effects. These latter effects are involved in the maintenance of cardiometabolic homeostasis (glucose and lipid metabolism as well as energy balance, and cardioprotection). Circulating and/or tissue levels of NGF and BDNF are altered in cardiometabolic diseases (atherosclerosis, obesity, type 2 diabetes, metabolic syndrome, and type 3 diabetes/Alzheimer's disease). A hypothesis thus emerged that a metabotrophic deficit due to the reduction of NGF/BDNF availability and/or utilization may be implicated in the pathogenesis of cariometabolic and neurodegenerative diseases. The present challenge is therefore to cultivate a metabotrophic thinking about how we can modulate NGF/BDNF secretion and signaling for the benefit of human cardiometabolic and mood health.Biomedical Reviews 2010; 21: 25-29

    Novel Interconnections in Lipid Metabolism Revealed by Overexpression of Sphingomyelin Synthase-1

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    This study investigates the consequences of elevating sphingomyelin synthase 1 (SMS1) activity, which generates the main mammalian sphingolipid, sphingomyelin. HepG2 cells stably transfected with SMS1 (HepG2-SMS1) exhibit elevated enzyme activity in vitro and increased sphingomyelin content (mainly C22:0- and C24:0-sphingomyelin) but lower hexosylceramide (Hex-Cer) levels. HepG2-SMS1 cells have fewer triacylglycerols than controls but similar diacylglycerol acyltransferase activity, triacylglycerol secretion, and mitochondrial function. Treatment with 1 mm palmitate increases de novo ceramide synthesis in both cell lines to a similar degree, causing accumulation of C16:0-ceramide (and some C18:0-, C20:0-, and C22:0-ceramides) as well as C16:0- and C18:0-Hex-Cers. In these experiments, the palmitic acid is delivered as a complex with delipidated BSA (2:1, mol/mol) and does not induce significant lipotoxicity. Based on precursor labeling, the flux through SM synthase also increases, which is exacerbated in HepG2-SMS1 cells. In contrast, palmitate-induced lipid droplet formation is significantly reduced in HepG2-SMS1 cells. [14C]Choline and [3H]palmitate tracking shows that SMS1 overexpression apparently affects the partitioning of palmitate-enriched diacylglycerol between the phosphatidylcholine and triacylglycerol pathways, to the benefit of the former. Furthermore, triacylglycerols from HepG2-SMS1 cells are enriched in polyunsaturated fatty acids, which is indicative of active remodeling. Together, these results delineate novel metabolic interactions between glycerolipids and sphingolipids

    SOS for Homo sapiens obesus

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    Published on 1 December 1994 issue of Nature, the Jeffrey Friedman's discovery "gave leptin in the beginning" of the endocrine saga of adipose tissue. Onwards, studies on this tissue have enjoyed an explosive growth that conceptualized a novel field of research, adipobiology. Arguably, in the heart of adipobiology and adipopharmacology are studies focusing on the pathogenesis, prevention and therapy of cardiometabolic diseases (CMD) including atherosclerosis, hypertension, obesity, type 2 diabetes, metabolic syndrome (global cardiometabolic risk), and lipodystrophies.Adipobiology 2010; 2: 5-8

    In the heart of adipobiology: cardiometabolic disease

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    Published on 1 December 1994 issue of Nature, the Jeffrey Friedman's discovery "gave leptin in the beginning" of the endocrine saga of adipose tissue. Onwards, studies on this tissue have enjoyed an explosive growth that conceptualized a novel field of research, adipobiology. Arguably, in the heart of adipobiology and adipopharmacology are studies focusing on the pathogenesis, prevention and therapy of cardiometabolic diseases (CMD) including atherosclerosis, hypertension, obesity, type 2 diabetes, metabolic syndrome (global cardiometabolic risk), and lipodystrophies.Biomedical Reviews 2009; 20: 1-5

    Social care costs for community-dwelling older people living with frailty

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    International evidence indicates that older people with frailty are more likely to access social care services, compared to nonfrail older people. There is, however, no robust evidence on costs of social care provided for community-dwelling older people living with frailty in their own homes. The main objective of this study was to examine the relationship between community-dwelling older people living with frailty, defined using the cumulative deficit model, and annual formal social care costs for the 2012–2018 period. A secondary objective was to estimate formal social care spending for every 1% reduction in the number of older people who develop frailty over 1 year. Secondary analysis of prospective cohort data from two large nationally representative community-based cohort studies in England was performed. Respondents aged ≥75 were used in the main analysis and respondents aged 65–74 in sensitivity testing. We used regression tree modelling for formal social care cost analysis including frailty, age, gender, age at completing education and living with partner as key covariates. We employed a minimum node size stopping criteria to limit tree complexity and overfitting and applied ‘bootstrap aggregating’ to improve robustness. We assessed the impact of an intervention for every 1% decrease in the number of individuals who become frail over 1 year in England. Results show that frailty is the strongest predictor of formal social care costs. Mean social care costs for people who are not frail are £321, compared with £2,895 for individuals with frailty. For every 1% of nonfrail people not transitioning to frailty savings of £4.4 million in annual expenditures on formal social care in England are expected, not including expenditure on care homes. Given considerably higher costs for individuals classed as frail compared to nonfrail, a successful intervention avoiding or postponing the onset of frailty has the potential to considerably reduce social care costs
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