Center for Simulation and Experimental Surgery, Faculty of Medicine, Pontificia Universidad Catolica de Chile, UC-Christus Health Network, Santiago, Chile.
Crystal J Trujillo's research spans surgical education, global health equity, and immunology. Her work uses AI to improve feedback quality in procedural training, examines inequities in childhood vaccination coverage, and investigates the cellular mechanisms of immune tolerance in autoimmune disease.
Kewalramani D, Roman DS, Lagos SA, Rammsy F, Villagran I +7 more
Plain English Researchers tested whether an AI tool called Teach1 could assess the quality of feedback given to medical students learning a bedside procedure, and whether better feedback led to better skill gains. Better-quality feedback correlated directly with improved performance scores, with every 10% improvement in feedback quality translating to about one additional point of skill improvement. The findings show that AI-graded feedback quality is a meaningful driver of learning, offering a scalable way to raise the standard of teaching across surgical training programs.
The Impact of COVID-19 Pandemic on Inequity in Routine Childhood Vaccination Coverage: A Systematic Review.
2022
Vaccines
Spencer N, Markham W, Johnson S, Arpin E, Nathawad R +4 more
Plain English This systematic review examined whether COVID-19 lockdowns widened existing inequities in routine childhood vaccination rates, analyzing studies from January 2020 through early 2022. Evidence from 13 studies found moderate-to-strong signals that vaccination coverage dropped more steeply for disadvantaged groups — particularly infants and children in middle-income countries — compared to pre-pandemic baselines. The findings highlight that public health crises can deepen vaccination gaps, with lasting consequences for the most vulnerable children.
Common causes for unsatisfactory Pap tests in a high-risk population: insights into a yet unresolved problem in gynecologic cytology.
2014
Journal of the American Society of Cytopathology
Quiroga-Garza G, Satrum LS, Trujillo CJ, Mody DR, Ge Y
Plain English This study analyzed 276 unsatisfactory Pap tests (out of 56,563) from a high-risk population to identify the most common reasons for inadequate results and determine follow-up risks. Low squamous cell count was the leading cause, most often in women over 50 with a history of gynecologic cancer, and nearly 30% of patients who had follow-up testing showed abnormal results. The high rate of subsequent abnormalities underscores the importance of diligent follow-up when a Pap test cannot be evaluated.
Gld mutation of Fas ligand increases the frequency and up-regulates cell survival genes in CD25+CD4+ TR cells.
2006
International immunology
Mohamood AS, Trujillo CJ, Zheng D, Jie C, Murillo FM +2 more
Plain English Researchers studied how a mutation that disables Fas ligand — a key protein for deleting unwanted immune cells — affects regulatory T cells (Tregs), which suppress autoimmunity. Despite the mutation causing a buildup of T cells, Tregs expanded disproportionately and retained their suppressive function, likely because they are normally hypersensitive to Fas-mediated death. This compensatory expansion of Tregs helps explain why Fas pathway defects paradoxically protect against certain autoimmune diseases rather than causing them.
B220+ double-negative T cells suppress polyclonal T cell activation by a Fas-independent mechanism that involves inhibition of IL-2 production.
2003
Journal of immunology (Baltimore, Md. : 1950)
Hamad AR, Mohamood AS, Trujillo CJ, Huang CT, Yuan E +1 more
Plain English This study showed that a population of unusual double-negative T cells that accumulate when the Fas immune deletion pathway is broken can suppress other T cells from proliferating and producing key immune-activating molecules. The suppression worked regardless of whether Fas signaling was present, required direct cell contact, and depended on the suppressor cells themselves being activated. These findings suggest that double-negative T cells serve as a backup system to prevent autoimmunity when the primary Fas-based deletion mechanism fails.