R
Raymond E. Galinsky
Researcher at Purdue University
Publications - 58
Citations - 1607
Raymond E. Galinsky is an academic researcher from Purdue University. The author has contributed to research in topics: Acetaminophen & Pharmacokinetics. The author has an hindex of 22, co-authored 58 publications receiving 1556 citations. Previous affiliations of Raymond E. Galinsky include Indiana University & Wishard Memorial Hospital.
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Hydrotropic polymeric micelles for enhanced paclitaxel solubility: in vitro and in vivo characterization.
TL;DR: The data suggest that polymeric micelles with a hydrotropic structure are superior as a carrier of paclitaxel due to a high solubilizing capacity combined with long-term stability, which has not been accomplished by other existing polymeric micelle systems.
Journal Article
Dose- and time-dependent elimination of acetaminophen in rats: pharmacokinetic implications of cosubstrate depletion.
Raymond E. Galinsky,Gerhard Levy +1 more
Journal Article
Use of N-acetyl cysteine to increase intracellular glutathione during the induction of antitumor responses by IL-2.
TL;DR: Oral NAc-cys administration significantly decreased tumor progression in a refractory s.c. tumor model and may be useful as an adjunct to increase the antitumor activity of IL-2/LAK therapy.
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Histamine N-methyltransferase pharmacogenetics : association of a common functional polymorphism with asthma
Lan Yan,Raymond E. Galinsky,Jonathan A. Bernstein,Stephen B. Liggett,Richard M. Weinshilboum +4 more
TL;DR: The association between a common, functionally significant genetic polymorphism for HNMT and asthma suggests that individual variation in histamine metabolism might contribute to the pathophysiology and/or response to therapy of this disease.
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Hepatic and intestinal cytochrome P450 3A activity in cirrhosis: effects of transjugular intrahepatic portosystemic shunts.
Naga Chalasani,J. Christopher Gorski,Nilesh H. Patel,Stephen D. Hall,Raymond E. Galinsky,Raymond E. Galinsky +5 more
TL;DR: In cirrhotic patients with TIPS, there was a marked loss in first‐pass metabolism of midazolam as a result of diminished intestinal CYP3A activity.