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Dr. Noriko Daneshtalab

Dr. Noriko Daneshtalab

Assistant Professor, Cross Appointment to Faculty of Medicine
norikod@mun.ca
Phone: 709 777 2218
H3422

Dr. Daneshtalab graduated from University of Alberta with her B.Sc. specializing in Pharmacology, and subsequently completed her PhD in 2005 also at the University of Alberta, Faculty of Pharmacy and Pharmaceutical Sciences. She majored in Pharmacokinetics and Pharmacodynamics of cardiovascular drugs in inflammatory states under Dr. Fakhreddin Jamali.

From 2004-2006, Dr. Daneshtalab completed her first post-doctoral training at the John P. Robarts institute for research in London, Ontario in Dr. Stephen Ferguson’s cell biology research group, characterizing GPCR signaling, membrane trafficking, and protein-receptor interaction and regulation.

Dr. Daneshtalab's second post-doctoral project began in 2007 under the guidance of Dr. John Smeda in the cardiovascular research group in the Division of Biomedical Sciences in Memorial University of Newfoundland. Her work investigated the multi-factorial mechanisms involved in hemorrhagic stroke development in the stroke-prone spontaneously hypertensive rats and methods of treatment.

Research Interest:

My intent is to study the Cardiovascular Pathogenesis Associated With Autoimmune Disease

I will develop an animal model that will study the effects of the co-existence of autoimmune diseases on the pathogenesis and cerebral vascular dysfunction associated with stroke. The pharmacokinetic and pharmacodynamic alterations of both cardiovascular and immuno-modulatory drugs will be studied with stroke development in the presence and absence of arthritis models.

The mechanisms of vascular dysfunction occurring with arthritis that lead to the development of stroke will also be investigated at the physiologic level. The role of the pro-inflammatory milieu in promoting therapeutic failure of cardiovascular drugs will also be assessed at the molecular level.

The studies will also involve both animal models and human patients recruited from across Canada to investigate the possible genetic component involved in causing the prevalence of cardiovascular disease in autoimmune patients and possible therapeutic implications associated with the co-existing diseases. In particular, I will be looking into prevalence of stroke in such patients.

The studies will apply and integrate molecular biology and physiology with a strong pharmacokinetic and pharmacodynamic base to understand the basis for changes to the cardiovascular system in an autoimmune disease, leading to altered drug response.

Select Publications:

Smeda JS, Daneshtalab N . "The effects of poststroke captopril and losartan treatment on cerebral blood flow autoregulation in SHRsp with hemorrhagic stroke." J Cereb Blood Flow Metab. 2010 Jul 21. [Epub ahead of print]

JS. Smeda, JJ. McGuire, N. Daneshtalab. "Protease-activated receptor 2 and bradykinin-mediated vasodilation in the cerebral arteries of stroke-prone rats." Peptides. 2010 Feb;31(2):227-37. Epub 2009 Nov 30.

N. Daneshtalab, JS. Smeda. "Alterations in the modulation of cerebrovascular tone and blood flow by nitric oxide synthases in SHRsp with stroke." Cardiovasc Res. 2010 Jan 19. [Epub ahead of print]

N.Daneshtalab, JJ. Doré, JS. Smeda. "Troubleshooting tissue specificity and antibody selection: Procedures in immunohistochemical studies." J Pharmacol Toxicol Methods. 2010 Mar-Apr;61(2):127-35. Epub 2009 Dec 24. Review.

N. Daneshtalab, A.S. Russell, R.Z. Lewanczuk, and F. Jamali. "Losartan Effect Is Not Down-Regulated by Rheumatoid Arthritis." J Clin Pharmacol. 2006 Nov; 46(11): 1344-1355

A. Policha, N. Daneshtalab, L.Chen, L.B.Dale, C. Altier, H Khosravani, W.G Thomas, G.W. Zamponi, S.S.G Ferguson. "Role of angiotensin II type 1A receptor phosphorylation, phospholipase D, and extracellular calcium in isoform-specific protein kinase C membrane translocation responses." J Biol Chem. 2006 Sep 8;281(36):26340-9. Epub 2006 Jul 10

N. Daneshtalab, R. Z.Lewanczuk, A. Russell and F. Jamali. "Rheumatoid arthritis does not reduce the pharmacodynamic response to valsartan ". J Clin Pharmacol. 2004; 4: 245-252.

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