Antonio Dávila, Ph.D.
Dr. Antonio Dávila Jr, Ph.D. is the Laboratory Director of the Penn Acute Research Collaboration (PARC) at Penn Presbyterian Medical Center. Dr. Dávila collaborates with Penn physicians and scientists to design and conduct clinical research and clinical trials on emergent and trauma patients. He works closely with the Trauma team, Surgical ICU team, and Emergency Medicine at Penn Presbyterian to enroll patients into the center’s myriad studies across clinical departments. PARC is a 24/7 collaborative acute care clinical research center with dedicated and specialized lab capacities that is unlike any other in the country.
“I encourage civic and research engagement from day one of my fall semester course. To reinforce concepts from the class, I regularly use examples from real-world clinical and research situations using videos and guest lectures presented by working nurses and all levels of nurse scientists. Based on student feedback, I am confident that this approach is successful at both engaging the students and exemplifying the aspects of teaching and learning that I believe are key for a career in any science. These are collaboration, creative and critical thinking, and the empowerment of students to be in charge of their own learning.”
- Ph.D., University of California, 2012
- M.S., University of California, 2004
- B.S., University of California, 2000
- B.A., University of California, 2000
For years, Dr. Dávila focused on understanding the molecular consequences that result from a traumatic injury, but the scope of his research has changed since having worked directly with the community as part of the TRACE project. In a retrospective study conducted by PARC on trauma patients admitted to the Penn Presbyterian Medical Center trauma bay between March 2017 and May 2019, it was discovered that 64.5% of these patients presented with an impaired ability to form blood clots because their platelets are not functioning properly.
This finding has led to a novel and collaborative line of research which focuses on answering the question: Why is the prevalence of platelet dysfunction (PD) so high in our trauma population? To address the etiology of this disorder, Dr. Davila’s lab is focusing on the patients’ living environment (i.e., home) as a principal contributor to the PD and to the increased mortality rates that plague our trauma patient population. They hypothesize that this is a direct consequence of a hyperactivated immune system resulting from the chronic environmental stress that these patients endure daily while living in low-income, high-crime, and violent areas of Philadelphia (where most of our patient population is from). This study seeks to understand the interdependencies of 1) the physical and social environment; 2) the psychological state as a function of increased environmental stress; 3) the hyperactive neural hormone stress response; and 4) the systemic immune hyperinflammation that creates the conditions for PD and poor medical outcomes.
A major goal for this project is to compel local, state, and federal governments to appropriate money and resources in these high-stress communities. We will argue that investment in these communities will not only increase the clinical outcomes of patients, but will also reduce the exorbitant costs of trauma- the burden of which falls largely on taxpayers. Indeed, crime, violence, and poverty are public health issues, but they also directly impact the health of individual people. Platelet dysfunction is a human vulnerability and the fact that is disproportionately affects low-income communities of color attests to the systemic mechanisms that maintain these health disparities. It is our goal to make healthcare and wellness equal for everyone, and revealing these insidious discrepancies is how we are contributing this movement.
Dr. Dávila is the Course Director for NURS061, Biologically-based Chemistry. This course takes a practical approach by relating the textbook chemistry material with real-world clinical and research situations using videos and guest lectures presented by working nurses and nurse scientists. Students are encouraged to engage in clinical or community research as an integral part of their academic career. Dr. Dávila has mentored undergraduate and graduate students and supports student trainees in his laboratory and field research.
In addition to his responsibilities at PARC, Dr. Dávila’s main areas of translational research investigates 1) NAD+ metabolism and mitochondrial bioenergetics in the immune cells of trauma patients and 2) the function and bioenergetics of apheresis platelets (PLT) in transfusion. The scope of his lab’s research includes not only understanding the molecular mechanisms underlying immunosuppression in trauma patients, but also seeks to address the chronic environmental stress conditions of our patient’s home life as a direct contributor to poor trauma patient outcomes.
Opportunities to Learn and Collaborate at Penn Nursing
In June 2020, Dr. Davila pivoted from his research to build a COVID-19 testing lab and establish Penn COVID TRACE, a community COVID-19 testing project. Since then, his team of volunteer nurses and students have provided free RT-PCR tests (48 hour results), blood antibody tests, and Rapid Antigen tests to persons in Philadelphia whom may not otherwise have access to these services. These include persons who are experiencing homelessness or drug addiction and as well as persons from immigrant or undocumented immigrant communities. The testing sites are located in Kensington, North Philadelphia, and West Philly. TRACE works closely with the Philadelphia Department of Public Health (PDPH) and non-profit groups to provide resources and information about COVID-19 and vaccinations. TRACE team members ask participants questions about their background and about their experiences during the pandemic. Further, to meet the needs of many study participants with substance use disorder, TRACE partners with Prevention Point Philadelphia and PDPH to provide harm reduction training and resources- including Narcan (naloxone nasal spray), Fentanyl test strips, PPE, sanitizers/cleaners, and gift cards (when applicable).
Warneford-Thomson R, Shah PP, Lundgren P, Lerner J, Morgan J, Davila A, Abella BS, Zaret K, Schug J, Jain R, Thaiss CA, Bonasio R. A. LAMP sequencing approach for high-throughput co-detection of SARS-CoV-2 and influenza virus in human saliva. (2022) eLife. 11:e69949. doi: 10.7554/eLife.69949
Procaccio V, Salazar G, Ono S, Styers M, Gearing M, Davila A, Jimenez R, Juncos J, Gutekunst CA, Meroni G, Fontanella B, Sontag E, J Sontag JM, Faundez V, Wainer BH. A mutation of β-actin which alters depolymerization dynamics is associated with autosomal dominant developmental malformations, deafness and dystonia. (2006) American Journal of Human Genetics. 78:947-960.
Potluri P, Davila A, Ruiz-Pesini E, Mishmar D, O’Hearn S, Hancock S, Simon M, Scheffler I, Wallace DC, Procaccio V. A novel NDUFA1 mutation leads to a progressive mitochondrial complex 1-specific neurodegenerative disease. (2009) Molecular Genetics and Metabolism.
Lim TS, Davila A, Wallace DC, Burke P. Assessment of mitochondrial membrane potential using an on-chip microelectrode in a microfluidic device.(2010) Lab on a Chip. 10(13):1683-8
Verni CC, Davila A, Sims CA, Diamond SL. D-Dimer and Fibrin Degradation Products Impair Platelet Signaling: Plasma D-Dimer Is a Predictor and Mediator of Platelet Dysfunction During Trauma. (2020) J. Appl Lab Med.5(6):1253-1264
Procaccio V, Neckelmann N, Paquis-Flucklinger V, Bannwarth S, Jimenez R, Davila A, Poole JC, Wallace DC. Detection of low levels of the mitochondrial tRNALeu(UUR) 3243A>G mutation in blood derived from patients with diabetes. (2006) Mol Diagn Ther. 2006;10(6):381-9
Torres MDT, de Lima LF, Ferreira AL, de Araujo WR, Callahan P, Dávila Jr A, Abella BS , de la Fuente-Nunez C. Detection of SARS-CoV-2 with RAPID: A prospective cohort study. (2022) iScience. 15;25(4):104055. DOI: 10.1016/j.isci.2022.104055
Davila A, Wallace DC. Epigenetic memory in the mitochondria of human embryonic stem cells. (2012) Mitochondrion. 12(5):581-582
Frederick DF, Davila A, Davis JG, Agarawal B, Michan S, Puchowicz MA, Nakamaru-Ogiso E, Baur JA. Increasing NAD Synthesis in muscle via nicotinamide phosphoribosyltransferase is not sufficient to promote oxidative metabolism. (2015) J. Biological Chemistry. 290(3):1546-58
Frederick DW, Loro E, Liu L, Davila A, Chellappa K, Silverman IM, Gosai SJ, Davis JG, Gregory BD, Dellinger RW, Redpath P, Migaud ME, Nakamaru-Ogiso E, Rabinowitz JD, Khurana TS, Baur JA. Loss of NAD homeostasis leads to progressive and reversible degeneration of skeletal muscle. (2016) Cell Metabolism. 24(2):269-282