个人简介
Dr. John H. McNeill completed a bachelor of science and a master of science in pharmacy at the University of Alberta, and a doctor of philosophy in pharmacology at University of Michigan.
Dr. McNeill was an assistant professor at Michigan State University (1967–1971), before coming to UBC in 1971, where he worked as associate professor and chairman in the Division of Pharmacology & Toxicology (1972–1975). Dr. McNeill became a professor in the Faculty of Pharmaceutical Sciences at UBC in 1975, and served as the Faculty's dean for 11 years (1985–1996). Dr. McNeill is no longer training new graduate students or providing undergraduate lectures.
研究领域
Dr. McNeill's research focuses on the effects of drugs on the heart. In particular, he has attempted to elucidate the biochemical mechanism of action of a number of drugs that produce a positive inotropic effect. He has also been interested in the mechanisms of action of drugs that interact with cardio stimulant agonists to enhance or block their effects.
His investigations on the effect of diabetes on rat hearts have revealed several biochemical, structural, functional and pharmacological differences. He has also found ways of treating the diabetes and preventing the cardiac changes in addition to insulin treatment. A more recent discovery has been that vanadium containing compounds lower blood glucose and prevent the secondary complications of diabetes in diabetic rats. He has recently synthesized and patented several compounds which have potential to be therapeutic agents. The finding that vanadium deposits in bone has led him to investigate if vanadium has positive or negative effects on bone structure. In the past several years he has studied the positive effects of beta blockade on the diabetic heart.
Dr. McNeill has developed rat animal models for the study of the metabolic syndrome, a syndrome characterized by hyperinsulinemia, insulin resistance and hypertension. He has shown that insulin-enhancing drugs will reduce all three of the above. These studies may lead to better treatments of hypertension by treating the root cause.
Diabetes produces deleterious changes in cardiac function in rats. There are significant alterations in cardiac metabolism, calcium handling and cell signaling that continue to be investigated. In addition, reactive oxygen species are increased in the diabetic state and contribute to the decrease in function. The cardiac muscle itself is damaged, a condition known as cardiomyopathy.
Dr. McNeill's model of the metabolic syndrome is the Fructose Fed Rat. Feeding rats a high fructose diet results in insulin resistance and hypertension which appear to be related. The work of his laboratory has shown an increase in activity of the sympathetic nervous system as well as in endothelin, angiotensin, thromboxane A2 and inflammatory factors. The presence of testosterone is also important in the development of the hypertension.
近期论文
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Testosterone-dependent increase in blood pressure is mediated by elevated Cyp4A expression in fructose-fed rats., Vasudevan, Harish, Yuen Violet G., and McNeill John H. , Mol Cell Biochem, 2012 Jan, Volume 359, Issue 1-2, p.409-18, (2012)
Inhibition of matrix metalloproteinase-2 improves endothelial function and prevents hypertension in insulin-resistant rats., Nagareddy, P R., Rajput P S., Vasudevan H, McClure B, Kumar U, Macleod K M., and McNeill J H. , Br J Pharmacol, 2012 Feb, Volume 165, Issue 3, p.705-15, (2012)
β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions., Sharma, Vijay, Sharma Arpeeta, Saran Varun, Bernatchez Pascal N., Allard Michael F., and McNeill John H. , Eur J Pharmacol, 2011 Apr 25, Volume 657, Issue 1-3, p.117-25, (2011)
The fructose-fed rat: a review on the mechanisms of fructose-induced insulin resistance and hypertension., Tran, Linda T., Yuen Violet G., and McNeill John H. , Mol Cell Biochem, 2009 Dec, Volume 332, Issue 1-2, p.145-59, (2009)
Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats., Heyliger, C E., Tahiliani A G., and McNeill J H. , Science, 1985 Mar 22, Volume 227, Issue 4693, p.1474-7, (1985)