Research

The following are research projects in which I have taken part listed in reverse chronological order.

Hospital Readmission Rates Following Telephonic Assessment After Discharge
LAC+USC Quality Improvement, Grant Winner from CIR/SEIU Quality Improvement Fund
Mentors: Dr Gina Rossetti, MD. Dr Eric Hsieh, MD.

From September 2015 until present, a group of residents and myself have been following patients with decompensated cirrhosis and congestive heart failure post-hospital discharge after randomly assigning them to either a post-discharge phone call group and a control group. The goal is to determine whether a post-discharge phone call with medication reconcilliation will reduce hospital readmission


Changes in Hand Coordination in Patients with Parkinson's Disease
Brain and Body Dynamics Lab, Viterbi School of Engineering, USC
Dr. Francisco Valero-Cuevas, PhD

From May 2012 until May 2014, I worked on a pilot study in the Parkinson's Disease population using novel technologies designed in the Valero-Cuevas lab in order to better quantify hand movements in hopes of finding a more efficient way to diagnose PD, determine prognosis, and determine efficacy of medications.

My poster for the 2013 Keck Required Student Project Fair can be found here.


Creating a Model for Retinoblastoma
Children's Hospital Los Angeles, The Vision Center
Dr. Thomas C. Lee, MD

From June 2010 until August 2011, I worked at Children's Hopital Los Angeles as a Research specialist in the Vision Center, developing a human model for Retinoblastoma. Retinoblastoma is a hereditary pediatric cancer of the eye and results from mutation of the Rb gene.  Although this is a rare tumor, the Rb gene is mutated in almost half of cancers.   As the human fetal retina is post-mitotic by week 22 of gestation, both copies of the gene are mutated prior to this time point, but the retinoblastoma tumor may not present until six months to five years of age.  The scientific community currently lacks an accurate model to better understand the progression of this disease from Rb mutation to tumor progression. Unfortunately, Rb+/- mice do not develop retinal tumors and so there is no animal model that accurately reflects this uniquely human cancer; therefore it is necessary to create a model using human tissue. Within this model, we can observe the earliest stages of the disease in vitro to better understand involved mechanisms.

My poster for the 2011 Saban Research Institute Poster Session can be found here.


Determining Cell Fate After DNA Damage
Center for Environmental Health Sciences, MIT
Dr. Leona Samson, Ph. D.

During the 2008-2009 school year, I worked in the Toxicology Lab at the Center for Environmental Health Sciences at MIT, working with two graduate students on their theses. The overall goal of the project is to create a model to accurately determine whether a cell will undergo cell death after DNA damage. We have been approaching this using a systems approach, observing two levels of regulation of the DNA damage response: protein signaling response and transcriptional response.

My focus was observing the protein signalling response. Once TK6 lymphoblastoids have been treated with MNNG, Western Blots were run with lysates and membranes were probed with various antibodies to discern protein signals. I created knockdown TK6 colonies through a new method of mammalian RNAi, which were to be mutagenized to observe protein signalling response.

This is my proposal for the Spring 2009 term.

 

Factors Influencing the Mechanism of Neural Progenitor Cell-Tumor Cell Binding
Department of Neuroscience, Beckman Research Institute, City of Hope Hospital
Dr. Mike Barish, Ph. D.

During the summers of 2007 and 2008, I worked at City of Hope in Duarte, California in the Neuroscience Laboratory. Our project was an offshoot of the breakthrough research done by Dr. Karen Aboody in stem cell therapeutics of cancer. Dr. Aboody's research dscovered a line of neuroprogenitor, HB1.F3, which preferentially targets tumor cells.

Our goal was to study the interaction of glioma and stem cells, using immunocytochemisty, labeling and inhibition experiments, in order to determine the mechanism to promote further advances in chemotherapuetics. Originally only U251 glioma cells were observed in culture with F3 neuroprogenitor cells. My project extended current research to breast cancer lines and identified a more reactive glioma.

This is my final report and my final presentation for Summer 2008.

 
 

 

 

 

spring
The spring. One of the devices used to measure strength and dexterity in the PD population. Patent held by Francisco Valero-Cuevas

 

 

 

iPS cells
An Rb +/- induced pluripotent stem cell colony from which retina can be derived

 

 

 


A Western Blot probing for Phosphorylated Jnk (Thr183/Tyr185) (greeg) and total Jnk (red). The first lane is the marker; the second 30ug untreated cell lysate. The other six lanes are treated with 500mM NaCl for 30 minutes and contain 5, 10, 20, 30, 40 and 50 ug of lysate.

 

 

 


A HB1.F3 neuroprogenitor (green) can be seen engulfing the U251 glioma (red). Through immunocytochemistry and cell labeling, the mechanism of this interaction was studied.