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Oxaliplatin-induced neuropathy in the rat: Involvement of oxalate in cold hyperalgesia but not mechanical allodynia
Effects of glutamate-related drugs on marble-burying behavior in mice: implications for obsessive-compulsive disorder.
First-pass metabolism of omeprazole in rats.
- K. Watanabe, K. Furuno, K. Eto, R. Oishi, Y. Gomita
- Medicine, BiologyJournal of pharmaceutical sciences
- 1 August 1994
It is suggested that omeprazole undergoes a first-pass metabolism in the intestinal mucosa and/or lumen, as well as in the liver, and that the major contribution to the dose-dependent increase in bioavailability is a saturation of the first- pass metabolism inThe liver.
Involvement of spinal NR2B-containing NMDA receptors in oxaliplatin-induced mechanical allodynia in rats
Results indicated that spinal NR2B-containing NMDA receptors are involved in the oxaliplatin-induced mechanical allodynia in rats, and nitric oxide synthase as a downstream target of NMDA receptor was examined.
Protection by a radical scavenger edaravone against cisplatin-induced nephrotoxicity in rats.
A simple and simultaneous determination of acyclovir and ganciclovir in human plasma by high-performance liquid chromatography.
- D. Teshima, K. Otsubo, Tsuneko Yoshida, Y. Itoh, R. Oishi
- ChemistryBiomedical chromatography : BMC
- 1 December 2003
A simple high-performance liquid chromatographic method was developed for the simultaneous determination of the therapeutic levels of acyclovir and ganciclovir in human plasma and is applicable to therapeutic monitoring during antiviral medication.
Neurotoxicity induced by tacrolimus after liver transplantation: relation to genetic polymorphisms of the ABCB1 (MDR1) gene
It is indicated that blood concentrations, liver function, graft weight, and polymorphism in the ABCB1 gene are important factors in tacrolimus-induced neurotoxicity.
Protective effect of cyclic AMP against cisplatin-induced nephrotoxicity.
Aripiprazole inhibits marble-burying behavior via 5-hydroxytryptamine (5-HT)1A receptor-independent mechanisms.
Amphotericin B-Induced Renal Tubular Cell Injury Is Mediated by Na+ Influx through Ion-Permeable Pores and Subsequent Activation of Mitogen-Activated Protein Kinases and Elevation of Intracellular…
It is suggested that Na+ entry through membrane pores formed by the association of AMB with membrane cholesterol leads to the activation of MAP kinases and the elevation of the intracellular Ca2+ concentration, leading to renal tubular cell injury.