Nikolova and Palatinus Win Clinical Fellows Award

"This year's finalists reflect the high-caliber research that is taking place here and the continued growth of Cedars-Sinai's research enterprise," said Mariko Ishimori, MD, assistant professor of Medicine, interim director of the Division of Rheumatology and the Cedars-Sinai site co-leader of the UCLA Clinical and Translational Science Institute (CTSI).

The two winners of the $3,000 prize, both of them cardiology fellows, were chosen from four finalists who presented summaries of their studies on April 10 to a panel of veteran Cedars-Sinai investigators in Harvey Morse Auditorium.

Nikolova's winning study was aimed at better managing patients diagnosed with a common but difficult-to-treat disorder—heart failure with preserved ejection fraction. This type of heart failure affects about half of heart-failure patients. It occurs when the heart muscle becomes so stiff that its pumping chambers can't properly fill with blood. 

Nikolova focused on the cBIN1 gene, which codes for proteins in the heart and regulates the strength of each heartbeat. She compared the cBIN1 levels in healthy laboratory rats with cBIN1 levels in rat models of heart failure with preserved ejection fraction. She also compared the cBIN1 levels in healthy volunteers with cBIN1 levels in patients with this disorder.

In both the patients and the rats with the disorder, levels of cBIN1 were markedly decreased. Nikolova concluded that a low level of cBIN1 correlates with worsening health of the heart muscle and may be useful in flagging the potential need for therapeutic intervention for heart failure with preserved ejection fraction.

Nikolova's mentor was TingTing Hong, MD, PhD, associate professor in the Cedars-Sinai Department of Medicine and research scientist at the Smidt Heart Institute.

Palatinus' winning study featured another vital organ, the kidney. He focused on acute kidney injury—sudden kidney failure or damage that happens within a few hours usually after blood flow to the kidney is decreased. This type of injury, which can be fatal, is observed in up to 10 percent of all hospitalized patients, and frequently is associated with diagnostic or therapeutic procedures. "There are yet to be developed pharmaceutical approaches that either prevent or treat acute kidney injury," Palatinus said.

Driven to address this void, Palatinus decided to explore applying research findings on the heart to the kidney. The heart findings came from the laboratory of his mentor Robin M. Shaw, MD, PhD. The Shaw team discovered that overexpression of a protein known as GJA1-20k could help protect the heart from damage. Palatinus hypothesized that GJA1-20k treatment could have a similarly protective impact on the kidney.

He first had to devise a means of delivering the protein to kidney cells. Once that hurdle was cleared, he analyzed GJA1-20k activity and found that it had a protective impact on kidney cells. Subsequently, Palatinus developed a model to replicate kidney injury in a mouse. Moving forward, he hopes to administer the GJA1-20k protein to the mice and determine whether the damage to the kidney in his model can be prevented. If he confirms that GJA1-20k is protective in the mouse model, Palatinus hopes to bring this protein to the bedside and use it to prevent or reduce kidney injury in susceptible patients.

The two other award finalists were Erica Cohen, MD, who presented "Noninvasive Digestion Monitoring With an FDA-Cleared Wearable Biosensor: Further Validation for Use in Tracking Food Ingestion," and Ma Ai Thanda Han, MD, who presented "Evaluating the Response to Placebo in Randomized Controlled Trials of Nonalcoholic Steatohepatitis: A Systematic Review and Meta-Analysis."

These awards are sponsored by the CTSI—which fosters clinical and translational science, education and training in the Los Angeles area and collaborative research among its four member institutions—and the Burns and Allen Research Institute.

The IACUC numbers for animal subjects referenced in this article are 5551 and 5280. The IRB numbers for human subjects in research referenced in this article are 32242 and 35991.