1,721,705 research outputs found
Nécrologie : Anne Dorne.
No full textVeyret Paul. Nécrologie : Anne Dorne.. In: Revue de géographie alpine, tome 41, n°2, 1953. pp. 159-160
Capra (Dr. Anna). — Variazioni periodiche della temperatura media a Bologna dal 1814 al 1933.
No full textDorne Anne. Capra (Dr. Anna). — Variazioni periodiche della temperatura media a Bologna dal 1814 al 1933. . In: Revue de géographie alpine, tome 28, n°3, 1940. pp. 465-467
Tous les combustibles sont rares : préparez-vous à l'hiver dès maintenant!
No full textCertaines sources font naître Albert Dorne en 1904. Inscription au crayon feutre dans le coin inférieur droit de l'affich
Towards next generation risk assessment of chemicals: Development and application of physiologically based kinetic models in farm animals
No full textContains fulltext :
219236.pdf (Publisher’s version ) (Open Access)Radboud University, 02 juni 2020Promotores : Ragas, A.M.J., Hendriks, A.J. Co-promotor : Dorne, J.L.C.M.126 p
The Effect of Lighting on Performance of Tasks Requiring Near Vision in Older Adults
No full textAbstract
Date Presented 4/1/2017
The study examined the impact of lighting on occupational task performance in older adults and the effect of lighting on perceived effort during task performance. Results suggest lighting may affect performance and perceived effort in older adults performing tasks requiring near vision.
Primary Author and Speaker: Karen James
Contributing Authors: Max Ito, Rachelle Dorne, JoAnne Wright</jats:p
Human variability in kinetics for the major metabolic pathways : Application to chemical risk assessment
No full textThis thesis deals with the statistical analysis of human variability in kinetics for the major metabolic pathways (Phase I (CYP isoforms (CYP1A2, CYP2C9, CYP2C19 CYP2D6, CYP2E1, CYP3A4), hydrolysis, Alcohol dehydrogenase). Phase n (N-acetyltransferases, glucuronidation, glycine conjugation, sulphation) and renal excretion) to investigate the appropriateness of the default uncertainty factor (10°^ 3.16) currently in use for the risk assessment of thresholded toxicants and accounting for human variability in kinetics. Probe substrates were selected on the basis that oral absorption was total and that the metabolic route was the primary route of elimination of the compound (60-100% of an oral). Intravenous data were used for compounds for which absorption was variable. Human variability in kinetics was quantified for each compound from published pharmacokinetic studies (after oral and intravenous dosing) in healthy adults and other subgroups of the population (effect of ethnicity, age and disease) using parameters relating to chronic exposure (metabolic and total clearances, area under the plasma concentration time-curve (AUG)) and acute exposure (Cmax). All parameters were analysed using the assumptions that data were either normally or log normally distributed and that kinetics were linear. Three sets of pathway-related uncertainty factors were calculated using the lognormal variability in kinetics to cover 95^, 97.5^ and 99"^ centile of the general healthy adult population respectively. These pathway-related uncertainty factors were also calculated for subgroups using the magnitude of the difference in internal dose between each subgroup and healthy adults (ratio of geometric means and the subgroup specific variability). Low inter-individual variability (about 21-31%) and pathway-related uncertainty factors (1.6- 2.2, 99*^ centile) were found for all monomorphic pathways with the exception of CYP3A4 metabolism for which variability after oral dosing was 46% (2.8, 99"^ centile). Polymorphic pathways showed that the current kinetic default would not be adequate to cover healthy adult poor metabolisers for CYP2D6 and CYP2C19 metabolism and slow acetylators for N-acetylation and uncertainty factors of 26, 52 and 5.2 would cover these</p
Polymorphic CYP2C19 and N-acetylation: human variability in kinetics and pathway-related uncertainty factors
No full textCYP2C19-mediated oxidation and N-acetylation constitute major phase I and phase II polymorphic pathways of xenobiotic metabolism in humans. Analysis of human variability in kinetics for these pathways has been carried out for compounds metabolised extensively (>60%) by these routes. Data for minor substrates for CYP2C19 metabolism (10–60%) have also been analysed. Published pharmacokinetic studies (after oral and intravenous dosing) in CYP2C19 non-phenotyped healthy adults (NPs), and phenotyped extensive (EMs), slow-extensive (SEMs) and poor metabolisers (PMs) have been analysed using data for parameters that relate primarily to chronic exposure (metabolic and total clearances, area under the plasma concentration–time curve) and primarily to acute exposure (peak concentration). Similar analyses were performed for the N-acetylation pathway using data for fast acetylators (FA) and slow acetylators (SA). Interindividual variability in the kinetics of CYP2C19 substrates after oral dosage was greater in EMs than in NPs (60 vs 43% for clearances and 54 vs 45% for Cmax). Lower variability was found for N-acetylation for both phenotypes (32 and 22% for FA and SA, respectively). The internal dose of CYP2C19 substrates in PM subjects would be 31-fold higher than in EMs, while for N-acetylated substrates there was a three-fold difference between SA and FA subjects. Pathway-related uncertainty factors were above the default safety factor of 3.16 for most subgroups and values of 52 and 5.2 would be necessary to cover to the 99th centile of the poor metaboliser phenotype for CYP2C19 and N-acetylation, respectively. An exponential relationship (R²=0.86) was found between the extent of CYP2C19 metabolism and the difference in internal dose between EMs and PMs. The kinetic default factor (3.16) would cover PMs for substrates for which CYP2C19 was responsible for up to 20–30% of the metabolism in EMs
Human variability in CYP3A4 metabolism and CYP3A4-related uncertainty factors for risk assessment
No full textCYP3A4 constitutes the major liver cytochrome P450 isoenzyme and is responsible for the oxidation of more than 50% of all known drugs. Human variability in kinetics for this pathway has been quantified using a database of 15 compounds metabolised extensively (>60%) by this CYP isoform in order to develop CYP3A4-related uncertainty factors for the risk assessment of environmental contaminants handled via this route. Data were analysed from published pharmacokinetic studies (after oral and intravenous dosing) in healthy adults and other subgroups using parameters relating primarily to chronic exposure [metabolic and total clearances, area under the plasma concentration–time curve (AUC)] and acute exposure (Cmax). Interindividual variability in kinetics was greater for the oral route (46%, 12 compounds) than for the intravenous route (32%, 14 compounds). The physiological and molecular basis for the difference between these two routes of exposure is discussed. In relation to the uncertainty factors used for risk assessment, the default kinetic factor of 3.16 would be adequate for adults, whereas a CYP3A4-related factor of 12 would be required to cover up to 99% of neonates, which have lower CYP3A4 activity
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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