Cornelis J. Van der Schyf

Abstract A number of phenols and aromatic ethers were deuterated in positions ortho and para to the phenolic groups using BF 3 etherate followed by quenching with Na 2 CO 3 in D 2 O. This method involves mild reaction conditions and should have wide applicability in the isotopic labeling of these compounds.

Boron trifluoride

10.1002/jlcr.2580241210

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Citations (7)

Mitochondrial ultrastructure and density in a primate model of persistent tardive dyskinesia

Life Sciences (2000)

Darryl W. Eyles Susan M. Pond Cornelis J. Van der Schyf Glenda M. Halliday

Tardive dyskinesia

Neuropil

Putamen

10.1016/s0024-3205(00)00442-2

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Citations (10)

Optimizing the use of open-source software applications in drug discovery

Drug Discovery Today (2006)

Werner J. Geldenhuys Kevin E. Gaasch Mark A. Watson David D. Allen Cornelis J. Van der Schyf

Cheminformatics

Perl

Python

10.1016/s1359-6446(05)03692-5

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Tobacco Smoke Chemicals Attenuate Brain-to-Blood Potassium Transport Mediated by the Na,K,2Cl-Cotransporter during Hypoxia-Reoxygenation

Journal of Pharmacology and Experimental Therapeutics (2005)

Jennifer R. Paulson Karen E. Roder Ghia McAfee David D. Allen Cornelis J. Van der Schyf

Smoking tobacco, including cigarettes, has been associated with an increased incidence and relative risk for cerebral infarction in both men and women. Recently, we have shown that nicotine and cotinine attenuate abluminal (brain facing) K(+) uptake mediated by the Na,K,2Cl-cotransporter (NKCC) in bovine brain microvessel endothelial cells (BBMECs) after hypoxic/aglycemic exposure (stroke conditions). The purpose of the current study was to explore the effects of nicotine and tobacco smoke chemicals on K(+) movement through the blood-brain barrier during both hypoxia/aglycemia and reoxygenation. BBMECs were exposed to nicotine/cotinine, nicotine-containing cigarette smoke extract (N-CSE), or nicotine-free cigarette smoke extract (NF-CSE) in quantities designed to mimic plasma concentrations of smokers. Stroke conditions were mimicked in vitro in BBMECs through 6 h of hypoxia/aglycemia with or without 12 h of reoxygenation, after which NKCC-mediated K(+) uptake and paracellular integrity were measured with (86)Rb and [(14)C]sucrose, respectively. In addition, K(+) concentrations in brain extracellular fluid were estimated in (86)Rb-injected rats that were administered nicotine, N-CSE, or NF-CSE and on whom global ischemia/reperfusion by in vivo four-vessel occlusion was performed. Both in vitro and in vivo paradigms showed nicotine, the major alkaloid present in tobacco smoke, to be the determining factor of an inhibited response of abluminal NKCC in BBMECs during and after stroke conditions. This was measured as a decrease in abluminal brain endothelial cell NKCC activity and as an increase in brain extracellular K(+) concentration measured as the brain extracellular fluid (86)Rb/plasma ratio after in vivo four-vessel occlusion with reperfusion.

Cotinine

Hypoxia

Tobacco smoke

10.1124/jpet.105.090738

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Citations (40)

Cornelis J. Van der Schyf

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