M
M. Strolin Benedetti
Researcher at UCB
Publications - 50
Citations - 1465
M. Strolin Benedetti is an academic researcher from UCB. The author has contributed to research in topics: Monoamine oxidase & Pharmacokinetics. The author has an hindex of 22, co-authored 50 publications receiving 1407 citations.
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Journal ArticleDOI
Drug metabolism and disposition in children
TL;DR: Key factors undergoing maturational changes accounting for differences in drug metabolism and disposition in the pediatric population compared with adults are reviewed and it would be important to generate information on the developmental aspects of renal P‐glycoprotein and of other renal transporters as done and still being done with the different isozymes involved indrug metabolism.
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Comparison of pharmacokinetics and metabolism of desloratadine, fexofenadine, levocetirizine and mizolastine in humans.
TL;DR: Fexofenadine is a P‐glycoprotein (P‐gp) substrate and P‐gp is certainly involved both in the poor brain penetration by the compound and, at least partially, in a number of observed drug interactions.
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Differences in absorption, distribution, metabolism and excretion of xenobiotics between the paediatric and adult populations
TL;DR: Key factors undergoing maturational changes accounting for differences in drug metabolism and disposition in the paediatric population compared with adults are reviewed and include glomerular filtration and tubular secretion.
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Dopamine-derived alkaloids in alcoholism and in Parkinson's and Huntington's diseases.
TL;DR: The changes in monoamine oxidase activity and the nigrostriatal concentrations of dopamine and homovanillic acid in Parkinson's and Huntington's diseases and in alcoholism are reviewed and the possible modifications found might cause or contribute to changes in mental and/or neurophysiological states in these pathological situations.
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Biosynthesis of salsolinol, a tetrahydroisoquinoline alkaloid, in healthy subjects.
TL;DR: The absence of salsolinol in the urine of one subject after Madopar administration seems to indicate that the biological system(s) involved in the reduction of the C = N bond in 1,2-dehydrosalsol can be missing or not, or poorly, functional in some individuals, and suggests that there is no alternative pathway for the formation of salolinol for healthy volunteers.