Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
5R01EY009178-05
Application #
2162818
Study Section
Visual Sciences B Study Section (VISB)
Project Start
1992-01-01
Project End
1996-12-31
Budget Start
1996-01-01
Budget End
1996-12-31
Support Year
5
Fiscal Year
1996
Total Cost
Indirect Cost
Name
Joslin Diabetes Center
Department
Type
DUNS #
071723084
City
Boston
State
MA
Country
United States
Zip Code
02215
Kuroki, Tatsuya; Isshiki, Keiji; King, George L (2003) Oxidative stress: the lead or supporting actor in the pathogenesis of diabetic complications. J Am Soc Nephrol 14:S216-20
Yokota, Tamotsu; Ma, Ronald C; Park, Joong-Yeol et al. (2003) Role of protein kinase C on the expression of platelet-derived growth factor and endothelin-1 in the retina of diabetic rats and cultured retinal capillary pericytes. Diabetes 52:838-45
Veves, A; King, G L (2001) Can VEGF reverse diabetic neuropathy in human subjects? J Clin Invest 107:1215-8
Way, K J; Katai, N; King, G L (2001) Protein kinase C and the development of diabetic vascular complications. Diabet Med 18:945-59
Meier, M; King, G L (2000) Protein kinase C activation and its pharmacological inhibition in vascular disease. Vasc Med 5:173-85
Park, J Y; Takahara, N; Gabriele, A et al. (2000) Induction of endothelin-1 expression by glucose: an effect of protein kinase C activation. Diabetes 49:1239-48
Mori, F; King, G L; Clermont, A C et al. (2000) Endothelin-3 regulation of retinal hemodynamics in nondiabetic and diabetic rats. Invest Ophthalmol Vis Sci 41:3955-62
King, G L; Wakasaki, H (1999) Theoretical mechanisms by which hyperglycemia and insulin resistance could cause cardiovascular diseases in diabetes. Diabetes Care 22 Suppl 3:C31-7
Ishii, H; Koya, D; King, G L (1998) Protein kinase C activation and its role in the development of vascular complications in diabetes mellitus. J Mol Med 76:21-31
Takagi, H; King, G L; Aiello, L P (1998) Hypoxia upregulates glucose transport activity through an adenosine-mediated increase of GLUT1 expression in retinal capillary endothelial cells. Diabetes 47:1480-8

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