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Biomedical subjects

R Kuhn

Publications and source records attributed to R Kuhn.

At least 199 records · Page 11Linked to original sources

Discovery and characterization of non-competitive antagonists of group I metabotropic glutamate receptors.

We have investigated the mechanism of inhibition of the new group I mGluR antagonists CPCCOEt and MPEP and determined that both compounds have a non-competitive mode of inhibition. Furthermore using chimeric/mutated receptors constructs we have found that these antagonists act at a novel pharmacological site located in the trans-membrane (TM). Specific non-conserved amino acid residues in the TM domain have been identified which are necessary for the inhibition by CPCCOEt and MPEP of the mGlul and mGlu5 receptors, respectively. Using molecular modeling a model of the TM domain was built for both mGlu1 and mGlu5 receptor subtypes. Docking of CPCCOEt and MPEP into their respective model allowed the modelisation of the novel binding site.

Binding Sites↗

Benefit of bicarbonate dialysis during CAVHD.

The effect of bicarbonate dialysate (BD) on acid-base status in six pediatric CAVHD patients was examined during seven episodes of metabolic acidosis. When metabolic acidosis was not corrected with CAVHD, a sterile BD was substituted for either acetate- or lactate-based dialysate. Pre- and post-BD substitution levels of lactate, HCO3, PCO2, anion gap, and pH were recorded, as well as dose of intravenous (i.v.) bicarbonate. Improvements in pH and serum HCO3 were seen in all seven cases. Anion gap decreased in all but one of the patients who were switched from lactate to bicarbonate dialysate, with improvement most marked in those patients with marked elevation of the anion gap. No adverse effect on PCO2 was noted. Lactate dialysate may be less effective when serum lactate levels are high, and may contribute to further elevation of lactate levels and anion gap. These data suggest that bicarbonate dialysate may be preferable to lactate or acetate dialysate in CAVHD patients with persistent metabolic acidosis.

Acid-Base Equilibrium↗