2013-2014 Yearlong Fellows

Stephen Villa

Project Title: How much information do we need to obtain at triage? A retrospective analysis of a novel approach to improve Emergency Department Quality of Care and Patient Satisfaction

Mentor(s): Ellen Weber, MD

Pathway: Clinical and Translational Research

Project Description: Emergency Department (ED) “crowding” is a complex issue today in the United States. Crowding is expected to worsen with the passage of the Affordable Care Act, and in response, EDs all over the country are looking for ways to improve patient flow. One process affecting throughput is triage.  Recent data has demonstrated that the traditional triage method delays recognition of acutely ill patients well beyond the recommended time frame in which they should be seen. We intend to study the impact of a streamlined triage method incorporated into a new electronic medical record system from both patient flow and safety perspectives. If we determine that the algorithm improves flow and is safe, it can be shared with many EDs as a means of expediting flow of patients, reducing crowding and improving patient safety and quality of care.

Why I do research: I have been interested in research since the early stages of my career as a means of affecting patients on a broader level. I eventually see myself at an academic institution working in an underserved population where I will have the opportunity to spend time as a clinician and a clinical researcher, investigating issues that directly affect these populations. This year will not only afford a better understanding of the research process and what it entails, but I believe will enhance a skill-set necessary to accomplish my future goals.

 

Daisy León-Martínez

Project Title: Differential gene expression in the Trisomy 21 placenta: elucidating functional deficits at the maternal-fetal interface

Mentor(s): Y. Katherine Bianco, MD, and Susan J. Fisher, PhD

Pathway: Molecular Medicine

Project Description: Embryonic aneuploidy is among the most common causes of miscarriage before 10 weeks of gestation. At this early stage, implantation and placentation are likely contributors to the demise of chromosomally abnormal embryos. However, little is known about the underlying mechanisms. An important body of knowledge has recently emerged from the Fisher Lab at UCSF regarding pathways required for normal placental formation and function. In the context of ongoing investigation, this study aims to explore gene expression patterns at the maternal-fetal interface in aneuploid pregnancies. Genes with potentially important functions have been identified and will be further studied in placentas of trisomy 21 pregnancies. Second, a novel trophoblast progenitor cell culture model of human placentation will be employed to investigate the functions of these molecules in normal and aneuploid pregnancy. Ultimately, enriching our knowledge of molecular consequences of the most common aneuploidy has the potential to yield better diagnostic and therapeutic approaches.

Why I do research: As someone with a growing interest in human embryonic/fetal development and high-risk obstetrics, I see this research fellowship as one of many steps towards building a career in academic medicine. In the short term, my work would involve employing molecular techniques to further investigate the functional consequences of Trisomy 21 in terms of the placenta. However, in a much broader context, this is a window through which we can better understand the mechanisms underlying the poor clinical outcomes affecting many of our patients.

 

Christopher Sanchez

Project Title: Hypoxic Preconditioning and the Unfolded Protein Response - A New Target For Neuroprotection Against Hypoxic Brain Injury

Mentor(s): Philip Bickler, MD, PhD

Pathway: Molecular Medicine

Project Description: Worldwide, stroke is among the top causes of death, accounting for an estimated 50 million lost disability-adjusted life-years (DALYs) by 2015. Present therapeutic strategies involve drugs that can dissolve clots, but no additional interventions exist to prevent or minimize the ischemic brain damage resulting from stroke. New fundamental knowledge is needed about the mechanisms which lead to neuronal injury and death to develop effective therapies for ischemic cerebrovascular disease. In the Bickler lab, I will investigate a process known as hypoxic preconditioning (HP), a rapid and reversible response to short durations of hypoxic conditions in which cells acquire protection against subsequent hypoxic or ischemic insults. Understanding HP therefore has great therapeutic potential and could provide further insight into neuronal cell death. I will be focusing on the unfolded protein response (UPR) which activates in response to ER stress and has been associated with hypoxic brain injury. I intend to study UPR signaling pathways and their effect on HP which may offer new targets to limit the neuronal injury related to ischemia.

Project Description: Since my first exposure to research in undergrad, I have been amazed at the ways we manipulate DNA and hijack cellular machinery to answer our questions. Having this background taught me that a career in medicine could be much larger than I had previously imagined. I do research because it serves the basis behind all the medicine we have learned these past 3 years and continuing the UCSF tradition of leading the research that drives the evolution of medicine is exciting, humbling, and will better equip me to pursue a career in academia.

 

Chelsea Young

Project Title: Child Care Asthma Preparedness Study

Mentor(s): Michael Cabana, MD, MPH, Anisha Patel, MD, MSPH, MSHS, and Curtis Chan, MD, MPH

Pathway: Health and Society

Project Description: How prepared are high-risk child care centers throughout San Francisco to prevent and manage asthma exacerbations among their children? My project represents a true collaboration between the UCSF Division of General Pediatrics and the Maternal Child and Adolescent Health Division of the San Francisco Department of Public Health. Working with DPH nurses, I will visit 42 high risk child care centers to look for common asthma triggers, interview child care managers about barriers to quality asthma care, and record how many children with asthma have appropriate medications and asthma action plans on site. At the end of this year, I hope to describe the state of asthma preparedness at these centers and suggest interventions that could be employed to address deficiencies. Moreover, I will work with the DPH to develop a tool that the public health nurses can use in the future to quickly assess child care centers for asthma preparedness.

Why I do research: Research enables us as clinicians to constantly improve the quality of care provided to our patients, a truly crucial pursuit. Every day, I am motivated by the fact that the findings that come out of my project will have an impact on DPH policy, thereby directly improving the lives of children throughout San Francisco. Asthma is a disease that disproportionately affects minority populations. My project represents one more step in the long path toward closing the gap in care that exists between racial groups in our city. I feel privileged to be allowed the opportunity to conduct this project.

 

Eric Dybbro

Project Title: Genetic and biochemical investigation into the ontogeny of Langerhans cell histiocytosis

Mentor(s): Michelle Hermiston, MD, PhD

Pathway: Molecular Medicine

Project Description: Langerhans cell histiocytosis (LCH) is a rare disorder of unknown etiology with diverse presentation that is characterized by accumulation of immature Langerhans cell (LC)-like dendritic cells (DCs). The spectrum of presentation can range from single-system disease, most commonly skin and bone, to diffuse multi-system involvement. Though current chemotherapeutic regimes are efficacious in many patients, those patients with high-risk multisystem disease have up to 20% mortality rate due to refractory or progressive disease despite systemic chemotherapy indicating a need for better understanding of the genetic underpinnings that underlies the diverse clinical presentations.  My research proposal aims to further explore the ontogeny of LCH though investigation of the presence of a genetic precursor as well as further elucidation of the cell-signaling pathways important in the pathogenesis of LCH.

Why I do research: I have been interested in research since the start of my medical training due to its role in advancing the field of medicine and have been amazed at both the speed and extent to which this dynamic field evolves. I am grateful to be able to participate in the Prof-Path yearlong fellowship as it represents a great opportunity to devote significant protected time to build my research skills and gain an in-depth understanding of the research process.

 

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