Catherine MacNary

Ms. Catherine MacNary


Research Focus & Metrics

Academic Career Length

1Year (2026-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Verified
Journal Article
Open access
PDF file
CMCatherine MacNary
Catherine MacNary
DBDimitrios E. Bakatsias
Dimitrios E. Bakatsias
GUGianna M. Ungaro
Gianna M. Ungaro
KSKrisha Suketu Shah
Krisha Suketu Shah
ALAda Liu
Ada Liu
Homaira M AzimHomaira M Azim
Homaira M Azim
Early clinical exposure (ECE) has been associated with increased confidence, professionalism, and career exploration in undergraduate medical education. Student-run free clinics (SRFCs), such as the Health Outreach Project (HOP) at Drexel University College of Medicine, provide opportunities for preclinical students to engage in patient care and community outreach. This qualitative study explored medical students’ perceptions of participation in HOP. Fourteen third- and fourth-year medical students with prior HOP experience participated in four semi-structured focus groups conducted virtually over Zoom. Data were analyzed using an inductive thematic analysis approach. Four major themes emerged: (1) early clinical exposure and clinical skills development, (2) community engagement and patient-centered perspectives, (3) professional identity formation and career exploration, and (4) opportunities, limitations, and emotional challenges of outreach work. Participants described HOP as an important source of authentic clinical exposure that increased confidence in patient interactions and broadened awareness of social determinants of health and underserved populations. Students also reflected on the influence of HOP on professional identity formation, career interests, and perspectives on patient-centered care, while acknowledging frustrations related to systemic barriers and limited resources. These findings suggest that students perceive SRFCs as valuable experiential learning environments that support clinical preparedness and professional development early in medical training.

3 July 2026 in Pathogens
Verified
Journal Article
Open access
PDF file
CMCatherine MacNary
Catherine MacNary
SGSai Chaitanya Rajendra Gaekwar
Sai Chaitanya Rajendra Gaekwar
ALAlexander Lemenze
Alexander Lemenze
ANAyaan Shiv Naik
Ayaan Shiv Naik
RTRitesh Tandon
Ritesh Tandon
PJPooja Jain
Pooja Jain
Human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic neuroinflammatory disorder often leading to demyelination of the spinal cord. Progression to HAM/TSP is closely associated with the high proviral load and the presence of virally infected CD4+ T cells that release extracellular vesicles (EVs). Exosomes, an EV subtype released by many cell types, transport proteins and nucleic acids that regulate intercellular communication and have been implicated in the progression of cancer and neuroinflammatory diseases. Herein, we have studied the effect of exosomes from HTLV-1 infected cells on the Peripheral Blood Mononuclear Cells (PBMCs) of HAM/TSP patients by single-cell sequencing utilizing innovative Honeycomb technology. We observed a distinct transcriptional response in monocyte populations compared with other immune cell types. Given that monocytes remain understudied in HTLV-1 pathogenesis, these findings highlight a potential role for infection-derived exosomes in shaping monocyte-driven immune dysregulation in HAM/TSP. A total of 41 genes were identified to be differentially expressed in HAM/TSP monocytes treated with exosomes; 28 were upregulated and 13 were downregulated. The most significantly altered genes are involved in chemokine activity and signaling, macrophage differentiation, lipid metabolism, and lysosomal function. Overall, our data suggests that exosome-treated HAM/TSP monocytes undergo immune remodeling that favors cell recruitment, activation, and a shift toward a mixed M1/M2-like phenotype. Such a shift may support viral persistence and chronic inflammation. These findings highlight a potential therapeutic pathway for addressing HTLV-1-induced neuroinflammation by modulating exosome-mediated signaling.