Postdoctoral Experience
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Northwestern University
Feinberg Cardiovascular Research Institute
Rishi Arora, MD
Gary Aistrup, PhD
Research Summary:
In this lab I studied atrial fibrillation in the presence of cardiac hypertrophy/heart failure. The presence of
heart failure alone increases the risk of developing atrial fibrillation, and those who have atrial fibrillation
and heart failure concurrently have a worse prognosis than those with heart failure alone. A common
occurrence in both conditions is amplified Gq signaling that results in increased intracellular calcium
and possible proarrhythmic calcium activity. I hypothesized that the increased calcium enters atrial
myocytes via canonical transient receptor potential channels (TRPCs). I was able to inhibit proarrhythmic
calcium activity in canine atrial myocytes using a Gq inhibitory peptide and TRPC inhibitors.
Northwestern University
Department of Urology
Olga Volpert, PhD
Research Summary:
I studied the natural inhibitor of angiogenesis called pigment-epithelial derived factor (PEDF). The lab
previously determined which part of the PEDF protein has these anti-angiogenic effects and synthesized
a peptide that contains only that region called 34mer. Using an array, I found several transcription factors
regulated by PEDF and 34mer. Many of the transcription factors that PEDF and 34mer activated are
known to control the cell cycle. My overall hypothesis was PEDF and 34mer blocks angiogenesis in
endothelial cells by regulating transcription factors that control cell division and proliferation, such as Rb,
C/EBPalpha and Ets-1. By studying the pathways PEDF utilizes, new therapeutic targets can be identified
and treatments developed to augment the effects of anti-angiogenic therapies in the treatment of cancer.
Feinberg Cardiovascular Research Institute
Rishi Arora, MD
Gary Aistrup, PhD
Research Summary:
In this lab I studied atrial fibrillation in the presence of cardiac hypertrophy/heart failure. The presence of
heart failure alone increases the risk of developing atrial fibrillation, and those who have atrial fibrillation
and heart failure concurrently have a worse prognosis than those with heart failure alone. A common
occurrence in both conditions is amplified Gq signaling that results in increased intracellular calcium
and possible proarrhythmic calcium activity. I hypothesized that the increased calcium enters atrial
myocytes via canonical transient receptor potential channels (TRPCs). I was able to inhibit proarrhythmic
calcium activity in canine atrial myocytes using a Gq inhibitory peptide and TRPC inhibitors.
Northwestern University
Department of Urology
Olga Volpert, PhD
Research Summary:
I studied the natural inhibitor of angiogenesis called pigment-epithelial derived factor (PEDF). The lab
previously determined which part of the PEDF protein has these anti-angiogenic effects and synthesized
a peptide that contains only that region called 34mer. Using an array, I found several transcription factors
regulated by PEDF and 34mer. Many of the transcription factors that PEDF and 34mer activated are
known to control the cell cycle. My overall hypothesis was PEDF and 34mer blocks angiogenesis in
endothelial cells by regulating transcription factors that control cell division and proliferation, such as Rb,
C/EBPalpha and Ets-1. By studying the pathways PEDF utilizes, new therapeutic targets can be identified
and treatments developed to augment the effects of anti-angiogenic therapies in the treatment of cancer.