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|Joint PhD Student Positions||DETAILS »|
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|Rodrigues Laboratory PhD Student Position||DETAILS »|
We are inviting enthusiastic students to apply for the joint PhD program in Pharmaceutical Sciences in the Faculty of Pharmaceutical Sciences at the University of British Columbia (lead university) and the Faculty of Health and Medical Sciences at the University of Copenhagen (partner university).
There are two openings for January 2015 start, one in drug delivery and the other in medicinal chemistry. Applications are sought from individuals with 1) a master's degree with excellent academic record and 2) interest and experience in the proposed research areas. Successful candidates will receive a stipend of $25,000/year for four years to study and conduct research between UBC and UCPH. A single doctoral degree will be awarded under the joint PhD agreement.
Enquires should be directed to Rachel Wu, graduate programs manager, at email@example.com and in the first instance should contain cover letter, CV and scanned copy of post-secondary transcripts. Please quote "joint PhD program" in the subject line of the email.
Applications are accepted until August 1, 2014 or until the positions are filled. All qualified candidates are encouraged to apply; however Canadians will be given priority.
We are actively seeking an individual who can join our laboratory as a PhD Student. Personnel specifications of the candidate include:
• A Masters degree
• Interest in biological research
• Excellent organizational ability and strong communication skills
• Experience in cell isolation, cell culture, Western Blotting, rtPCR and enzymology
Heart has a limited potential to synthesize fatty acid (FA) and therefore FA is supplied from several sources: lipolysis of endogenous cardiac triglyceride (TG) stores, or from exogenous sources in the blood. Lipoprotein lipase (LPL), synthesized in cardiomyocytes, catalyzes the breakdown of the TG component of lipoproteins to provide FA to the heart. It is the vascular endothelial-bound LPL that determines the rate of plasma TG clearance and hence, it is also called heparin releasable (HR) "functional" LPL. Functional LPL is regulated by numerous dietary and hormonal factors, and is sensitive to pathophysiological alterations like those observed during diabetes. In this condition, absolute or relative lack of insulin impairs cardiac glucose transport and oxidation, resulting in FA becoming the preferred means of energy supply. To make available this increased requirement of the heart for FA, diabetic heart upregulates its luminal LPL activity by posttranslational mechanisms. Chronically elevated cardiac LPL can result in abnormal FA supply and utilization by the heart tissue that could potentially initiate and sustain cardiac dysfunction during diabetes. The student recruited will be expected to examine the regulation of cardiac LPL in an attempt to piece together how early metabolic changes could instigate diabetic heart disease.
1. Kim, M.S., Wang, F., Puthanveetil, P., Kewalramani, G., Hosseini-Beheshti, E., Ng, N., Wang, Y., Kumar, U., Innis, S., Proud, C.G., Abrahani, A., and Rodrigues, B. Protein kinase D is a key regulator of cardiomyocyte lipoprotein lipase secretion after diabetes. Circ. Res. 103: 252-260, 2008.
2. Kim, M.S., Kewalramani, G., Puthanveetil, P., Lee, V., Kumar, U., An, D., Abrahani, A, and Rodrigues, B. Acute diabetes moderates trafficking of cardiac lipoprotein lipase through p38 MAPK dependent actin cytoskeleton organization. Diabetes 57: 64-76, 2008.
3. Kim, M., Wang, F., Puthanveetil, P., Kewalramani, G., Marzban, L., Steinberg, S.F., Webber, T.D., Kieffer, T.J., Abrahani, A., and Rodrigues, B. Cleavage of protein kinase D following acute hypoinsulinemia prevents excessive LPL-mediated triglyceride accumulation. Diabetes 58: 2464-2475, 2009.
4. Wang, Y., Puthanveetil, P., Wang. F., Kim, M. S., Abrahani, A., and Rodrigues, B. The severity of diabetes governs vascular LPL by affecting enzyme dimerization and disassembly. Diabetes. 60:2041-2050, 2011.
5. Wang, F., Wang, Y., Zhang, D., Puthanveetil, P., Johnson, J.D., Abrahani, A., and Rodrigues, B. Fatty acid-induced nuclear translocation of heparanase uncoupels glucose metabollism in endothelial cells. Arterioscler. Thromb. Vasc. Biol 32: 406-414, 2012.
Interested individuals are requested to submit a letter of research interests and current CV to:
Rachel Wu, Graduate Programs Manager
Faculty of Pharmaceutical Sciences
The University of British Columbia
174-2146 East Mall, Vancouver, BC, Canada V6T 1Z3