United States

Background
Chronic alcohol exposure impairs both the systemic and intestinal immune system. In humans, alcohol use disorder increases sepsis mortality. However, the mechanisms by which alcohol impacts immune dysregulation during sepsis are not well understood. We previously showed that alcohol downregulates the integrin CD103 on regulatory T cells (Tregs), a highly specialized immunosuppressive T cell population, in non-septic mice. We hypothesized that alcohol-induced changes in CD103 signaling on Tregs would increase sepsis mortality. 
Methods
To model chronic alcohol ingestion, B6 mice were randomized to drink either water or alcohol for 12 weeks. At 18-22 weeks, mice underwent cecal-ligation-and-puncture (CLP) to induce polymicrobial intraabdominal sepsis. Mice were sacrificed after 24 hours, and single cell suspensions were prepared from the spleen, lungs, and small intestine for flow cytometric analysis. Comparisons between groups were analyzed using Student’s T Test or Mann Whitney Test. For survival analysis, sex-matched B6 mice underwent CLP. Mice were randomized to receive injections of CD103 blocking antibody or control postoperatively. For Treg depletion, mice received injections of anti-CD25 prior to and at the time of CLP. Mice were followed for seven days, and their survival was compared using Kaplan-Meier curves.
Results
Frequencies of T cell populations in the spleen, lung, and intestine of septic water-fed versus alcohol-fed mice were assessed by flow cytometry. Compared to water-fed mice, alcohol-fed mice had lower frequencies of CD103+Foxp3+CD4+Tregs in the spleen (p=0.0004), lungs (p=0.008), small intestine epithelium (p=0.0004) and lamina propria (p=0.0002). Compared to CD103- Tregs, CD103+ Tregs had higher expression of activation markers (CD44, CD69) and immunosuppressive molecules (CTLA4, PD1, CD39, CD73, TIGI), whereas CD103- Tregs expressed higher levels of a naïve circulating marker (CD62L) and transcription factor associated with the pro-inflammatory Th17 phenotype (RORyt). Tregs from the epithelium of septic alcohol-fed mice expressed higher levels of CD44 (p=0.02) and RORyt (p=0.04) than those from water-fed mice. CD103 blockade significantly increased sepsis mortality in water-fed mice (p=0.03), but did not affect survival in alcohol-fed or Treg-depleted mice. 
Conclusion
Alcohol causes a shift in the Treg population by decreasing the frequency of the highly immunosuppressive CD103+Treg subset during sepsis and a change in Treg phenotype in the small intestine epithelium. CD103 signaling has a protective effect in sepsis. This effect is mediated, in part, by Tregs and eliminated by chronic alcohol exposure. Alcohol-induced downregulation of CD103 on Tregs therefore contributes to immune dysregulation in sepsis.

AMA Research Challenge 2025 

Effect of Alcohol-Induced Downregulation of Integrin CD103 on Immune Dysregulation in Sepsis

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poster

Objective / Hypothesis: Type 1 Diabetes involves autoimmune destruction of pancreatic β-cells, likely driven by genetic predisposition and environmental factors such as enteroviral infections. Autophagy, a cellular stress response pathway, is impaired in T1D and may influence immune recognition of β-cells. We hypothesized that modifications in β-cell autophagy, with or without viral infection, may alter human islet HLA-I expression and potentially specific HLA-I isotypes, with broader implications for altered β-cell immunogenicity.

Approach: Human pancreatic islets were infected with Coxsackievirus B3, a common
enterovirus, and treated with either Bafilomycin A1 or C381 (autophagy inhibitor or enhancer, respectively). We assessed the impacts of aberrant autophagy on the surface expression of total and specific HLA-I isotypes to evaluate the impact of autophagy modulation on antigen presentation in β-cells.

Summary / Conclusions: We demonstrated that autophagy inhibition led to increased HLA-I expression in human islets, whereas autophagy stimulation reduced expression. In addition, we found that there are altered expression patterns of specific HLA-I isotypes under conditions of impaired autophagy, suggesting that autophagy plays a regulatory role in shaping β-cell antigenic presentation, with implications for T1D development and progression.

Autophagy-Driven Modulation of HLA Class I in Coxsackievirus B Infected Human Pancreatic β-Cells

Background 
Diabetic retinopathy (DR) is a leading cause of vision loss in patients with diabetes mellitus due to damage of the retinal microvasculature, primarily involving retinal endothelial cells (HRECs) and pericytes (HRPs). HRPs regulate vascular stability, while HRECs maintain the blood-retina barrier. Dysfunction in these cells leads to retinal vascular leakage, pathologic neovascularization, and vision loss. Small extracellular vesicles (sEVs) are membrane bound nanoparticles that mediate intercellular signaling and have been implicated in DR-related vascular damage. While sEVs contribute to oxidative stress and angiogenesis, the role of retinal pericyte-derived sEVs on retinal endothelial dysfunction under diabetic stress remains unclear. This study investigates the impact of pericyte-derived sEVs on endothelial barrier integrity, metabolism, and angiogenic activity.

Methods
HRPs were cultured in conditioned media under high glucose and hypoxic conditions as a diabetic condition, or mannitol and normoxic conditions as a control. The HRP cell medium was then collected after 48 hours, and the sEVs were obtained using the EXODUS exosome isolation system. sEV size distribution and concentration was assessed using a nanoparticle tracking analyzer (NTA) instrument which measured sEV hydrodynamic diameter and concentration. sEV morphology was confirmed using transmission electron microscopy (TEM). HRECs were then treated with the HRP derived sEVs, and functional assays were conducted. Trans-endothelial electrical resistance (TEER) was measured with cell-covered electrodes and endothelial cell permeability was measured with fluorescently labeled tracer dye diffusion across an HREC monolayer on a Transwell insert. Additional assays included MTT-based metabolic activity and scratch wound migration to assess angiogenesis.

Results
Nanoparticle tracking analysis showed no significant differences in sEV size or concentration between the two conditions. Transmission electron microscopy showed no differences in sEV structure and morphology between the two conditions. However, sEVs from diabetic-stressed HRPs significantly reduced HREC trans-endothelial resistance (TEER) and increased HREC permeability in Transwell assays compared to the control. This suggests compromised barrier integrity in retinal blood vessels. At lower sEV doses, metabolic assays showed higher HREC viability in response to control HRP-derived sEVs compared to high glucose HRP-derived sEVs. Cell migration assays revealed that HRECs treated with diabetic stress HRP sEVs exhibited faster growth, consistent with angiogenesis and neovascularization in DR.

Conclusion 
These findings suggest that sEVs from HRPs under diabetic stress promote retinal vascular permeability and endothelial dysfunction, contributing to DR pathogenesis. Targeting sEV release could provide a novel therapeutic approach for preventing or treating DR. Further research is needed to elucidate the mechanisms involved and potential clinical benefits.


Retinal Pericyte-Derived Small Extracellular Vesicles Induce Endothelial Dysfunction under Diabetic Stress

Background
The frequent use of systematic aminoglycoside (AG) treatment has resulted in a widespread trend of permanent hearing loss globally. Previously, we found that AGs induce a rapid translocation of RIPOR2 in hair cells, which is a process that relies on functional mechanotransduction and subsequently dysregulates the autophagy/mitophagy pathway, leading to irreversible hair cell death. Recent studies found that AGs also trigger rapid phosphatidylserine (PS) externalization in hair cells, possibly by activating the scramblase activity of TMC1/2, which are the pore-forming subunits of the mechanotransduction channel. Since both processes are AG-triggered and mechanotransduction-dependent, we investigated if RIPOR2 translocation and PS externalization occurred through dependent pathways.

Methods
To determine whether AG-triggered rapid RIPOR2 translocation and PS externalization are dependent, RIPOR2 translocation and PS externalization were observed with fluorescent microscopy in wild-type hair cells treated with gentamycin. Tmie -/- cochlea were also treated with gentamycin to investigate the role of core mechanotransduction channel proteins TMC1/2 in the aforementioned processes. To study the effect of PS externalization on RIPOR2 translocation in hair cells, we treated wild type cells with Benzamil, which induces PS externalization through MET channel blockage. Finally, we treated wild type hair cells with cisplatin, a drug that shares several pathological features of ototoxicity with AGs, to observe its effects on PS externalization and RIPOR2 localization in hair cells.

Results
Gentamycin can trigger both RIPOR2 translocation and PS externalization in wild type mice, but not in Tmie -/- mice. Throughout the 2-hour gentamycin treatment, PS externalization and RIPOR2 translocation displayed distinct spatiotemporal distributions. We found that Benzamil, which is sufficient to trigger PS externalization, was unable to trigger RIPOR2 translocation under our experimental conditions. In addition, we observed that cisplatin treatment, unlike gentamycin treatment, was unable to trigger either RIPOR2 translocation or PS externalization. 

Conclusion
Aminoglycoside treatment likely triggers RIPOR2 translocation and PS externalization via independent mechanisms, considering that both phenomena display distinct spatiotemporal patterns with gentamycin treatment, and certain MET-blocking reagents that induce PS externalization (e.g. Benzamil) fail to induce RIPOR2 translocation. However, the failure for gentamycin to induce either phenomenon in Tmie -/- cells suggests that the MET channel plays a significant role in the function of both pathways. Because cisplatin could neither induce PS externalization nor RIPOR2 translocation, it is probable that cisplatin triggers hair cell death through a pathway distinct from that of aminoglycoside-mediated ototoxicity. 


Aminoglycoside induces RIPOR2 Translocation and Phosphatidylserine Externalization via Distinct Mechanisms

Stress is ubiquitous in the practice of medicine. The way individuals view stress is known to have an impact on stress itself. It is an emotion that is widely viewed as negative by many; to minimize this perspective, various studies have indicated that viewing stress positively in a way that can promote growth, and resilience has been associated with better well-being. Our cross-sectional study aimed to examine relationships between stress mindset, resiliency, grit, and burnout in several Wright State University (WSU) residency programs. A survey was sent to 204 residents in Emergency Medicine, Family Medicine, Internal Medicine, and Surgery, consisting of the following measures: Stress Mindset Measure (SMM), Grit Scale, Mini ReZ Survey (burnout, stress, and resilience), and adverse childhood events (ACEs). Completed surveys were received from 85 residents (41.7% response rate). There was a large positive correlation between stress mindset and burnout (rs = 0.50, p <.0001). An ordinal logistic regression modeled the odds of increasing burnout and found a significant relationship between stress mindset and burnout (odds ratio = 0.779; 95% confidence interval = 0.695 – 0.866). For a one-unit increase in stress mindset (i.e., viewing stress more positively), the odds of higher levels of burnout decreased by 22.0%. Grit and the number of ACEs were not significantly related to burnout. Our cross-sectional study of WSU residents reveals a significant inverse relationship between stress mindset and burnout, suggesting that viewing stress more positively is associated with lower odds of experiencing burnout. Specifically, a one-unit increase in stress mindset was associated with a 22% decrease in the odds of higher levels of burnout. Interestingly, grit and the number of adverse childhood experiences were not found to be significantly related to burnout in this cohort. These findings underscore the potential importance of fostering a positive stress mindset as a modifiable factor in mitigating burnout among medical residents. Further longitudinal research is warranted to explore the causal nature of this relationship and to develop targeted interventions aimed at cultivating a more adaptive stress mindset in this high-stress professional population.


The Role of Stress Mindset in Burnout and Resilience Among
Medical Residents: A Cross-Sectional Study

Background:
Adverse Childhood Experiences (ACEs) are stressful events in early life (neglect, parental substance abuse, household mental illness, etc.) that are associated with an increased lifetime risk for chronic diseases, including cardiovascular disease (CVD). It is estimated that 64% of US adults have at least one ACE and 17% have four or more ACEs. Endothelial dysfunction is a key early marker of cardiovascular disease and may provide insight into subclinical vascular changes. This study aimed to investigate whether exposure to ACE’s is associated with impaired endothelial function in young, apparently healthy adults.
Methods:
Twenty-nine young adults (ages 18–29), apparently healthy, were stratified into high (>4 ACEs; n=14) and low (≤4 ACEs; n=15) ACE exposure based on the self-reported standardized ACE questionnaire. Endothelial function was assessed using brachial artery flow-mediated dilation (FMD), a validated, noninvasive ultrasound technique that measures vascular response at rest, occlusion, and post-occlusion. Additional physiological measures were collected, including body mass index (BMI), systolic and diastolic blood pressure, heart rate, C-reactive protein (CRP), and hemoglobin A1c (HbA1c). Group comparisons were performed using independent t-tests, with p < 0.05 considered statistically significant.
Results:
Participants who reported a high number of ACEs presented with significantly lower FMD compared to those who experienced lower numbers of ACEs (> 4 ACEs: 6.7 ± 4.0% vs. ≤4 ACEs: 10.6 ± 5.0 %; p = 0.041), indicating reduced endothelial function. When normalized to shear rate, FMD remained significantly lower in the high ACE group (> 4 ACEs: 0.2 ± 0.1 vs. ≤4 ACEs: 0.4 ± 0.3; p = 0.030). Baseline artery diameter (p = 0.242), peak diameter (p = 0.503), and diameter during occlusion (p = 0.277) were similar between the groups. Additionally, no significant differences were observed in physiological parameters (BMI, SBP, DBP, HR, CRP, and HbA1c).
Conclusion:
These results demonstrate that young, apparently healthy adults with a history of increased childhood adversity exhibit reduced endothelial function, an early marker of CVD development and increased CVD risk. Estimates, based on previous literature, show that a 3.9% reduction in the FMD test as observed in the high ACE group may correspond to an estimated 34% increased future CVD risk. These findings support existing literature suggesting that adversity early in life may serve as a subclinical indicator of increased risk of premature CVD potentially identifying vulnerability before traditional clinical markers emerge.

Endothelial Health After Adversity: How Childhood Adversity May Increase Cardiovascular Risk

Background
Unrecognized myocardial infarction (UMI) is associated with higher mortality compared with no myocardial infarction (MI) in both asymptomatic individuals and symptomatic patients suspected
of having coronary artery disease (CAD) undergoing cardiac testing. We aimed to understand the mechanisms underlying the higher mortality associated with UMI.

Methods
We conducted a retrospective cohort study of consecutive patients with obstructive CAD who underwent clinical cardiovascular magnetic resonance imaging (CMR). Patients were classified into 4 groups based on their history of MI (HxMI) and the presence of MI on CMR (CMRMI): +CAD,-HxMI,+CMRMI; +CAD,+HxMI,+CMRMI; +CAD,+HxMI,-CMRMI; and +CAD,-HxMI,-CMRMI. Outcomes included all-cause death, non-fatal MI or death due to MI, heart failure (HF) hospitalization or death due to HF, and sudden cardiac death (SCD). Statistical analyses included Kaplan-Meier survival analysis, Cox proportional hazards regression, and Fine-Gray competing risks modeling.

Results
Among 2,511 +CAD patients, 933 (37%) had -HxMI. Of these, 59% had +CMRMI. Over a median follow-up of 6.4 years, +CAD,-HxMI,+CMRMI patients had higher mortality compared with +CAD,-HxMI,-CMRMI patients (hazard ratio 1.62; 95% confidence interval 1.26-2.09; p<0.001). Furthermore, +CAD,-HxMI,+CMRMI patients experienced more HF events than +CAD,-HxMI,-CMRMI patients. However, there were no significant differences in MI events or SCD. Among +CAD,+HxMI patients, 14% had -CMRMI, and their mortality was not different from that of +CAD,-HxMI,-CMRMI patients.

Conclusion
+CAD,-HxMI,+CMRMI patients had higher mortality than +CAD,-HxMI,-CMRMI patients, primarily due to greater HF events. While both CAD-related and myocardial disease related outcomes contribute to the higher mortality associated with UMI, the primary mechanism is HF outcomes.

Long-term Outcomes of Unrecognized Myocardial Infarction in Patients With Coronary Artery Disease

Background:
Lipid profiles (LP) are commonly used to assess cardiovascular disease (CVD) risk, yet they do not differentiate between LDL subtypes. Lipoprotein(a) [Lp(a)] is a highly atherogenic LDL variant with pro-inflammatory and pro-thrombotic properties that significantly contribute to atherosclerosis and vascular inflammation. Despite its clinical relevance, Lp(a) is frequently overlooked, and its elevated levels—present in 20–30% of the population—pose an independent risk for CVD, even when LDL-C is within normal ranges. The underutilization of Lp(a) testing may contribute to missed opportunities for early risk stratification. This study examines the utility of integrating Lp(a) testing into routine cardiovascular risk assessments, particularly for certain at-risk populations. It evaluates the frequency of physician-ordered Lp(a) testing, the prevalence of elevated Lp(a) levels, and its implications for otherwise healthy individuals.
Methods:
A systematic literature review of various study types was conducted to assess research on Lp(a) testing patterns, prevalence, and its association with CVD risk. PubMed, Google Scholar, and OpenEvidence were utilized. Keywords used in the search included “Lipoprotein(a),” “cardiovascular risk,” “CVD biomarkers,” and “ordering pattern.” Studies not focused primarily on Lp(a) were excluded.
Results:
One study found that only 1% of patients in a large northern California health system underwent Lp(a) testing between 2010 and 2021, while another reported that just 31% of physicians routinely assessed Lp(a) levels. Elevated Lp(a) was observed in 20–30% of individuals, and even among those with LDL-C <100 mg/dL, Lp(a) levels >50 mg/dL were associated with increased atherosclerotic cardiovascular disease (ASCVD) risk. A key limitation of this study is the lack of consideration for the cost of Lp(a) testing, which may impact physician ordering patterns and accessibility for patients.
Conclusion:
Standard LDL-C evaluation alone may be insufficient for comprehensive CVD risk assessment. Given the strong association between elevated Lp(a) and CVD, routine testing in at-risk populations is warranted to improve early detection and intervention strategies. 


Lipoprotein (a) as a key biomarker for a comprehensive cardiovascular risk assessment

Background:
Mycosis fungoides (MF) is the most common variant of cutaneous T-cell lymphoma, a heterogeneous group of non-Hodgkin lymphomas that primarily affect the skin. Narrowband UVB (NB-UVB) phototherapy is a first-line treatment for early-stage MF across Fitzpatrick skin types (FSTs). However, existing NB-UVB guidelines are largely derived from studies with limited skin type diversity. In a 2023 pilot study, our group demonstrated that MF patients with higher FSTs experience slower improvement on NB-UVB. Here, we validate and expand these findings using a multicenter cohort.

Methods:
We conducted a retrospective chart review of MF patients at Columbia, Johns Hopkins, and Emory Universities who underwent NB-UVB monotherapy between January 2010 and June 2025. Patients were included if they had demonstrable disease within 90 days of NB-UVB initiation and at least two documented disease severity assessments (measured as % total body surface area [TBSA] involved). Patients receiving concurrent systemic therapy and radiation were excluded. Patients were stratified by FST (I-III vs IV-VI).

Timepoints were categorized as baseline, mid-year, year-end, and end of follow-up. The primary outcome was the change in TBSA involvement at each timepoint. Statistical analyses included Chi-square and Fisher’s exact tests for categorical variables, and Wilcoxon rank-sum and Welch t tests for continuous variables; α = 0.05.

Results:
A total of 114 patients (63 FST I-III, 51 FST IV-VI) met inclusion criteria. Baseline demographic and disease characteristics differed between groups: patients with FST IV-VI were younger (mean age 49 vs 60 years, p < 0.001) and more likely to present with hypopigmented MF (43% vs 4.8%, p < 0.001). Patients with FST I-III experienced significantly greater percent reductions in TBSA than those with FST IV-VI, with reductions of 73% versus 35% at mid-year (p = 0.009), 78% versus 26% at year-end (p = 0.009), and 78% versus 47% at end of follow-up (p = 0.006). Absolute TBSA reductions mirrored these trends, with greater improvement observed in FST I-III at year-end (−14 vs −10, p = 0.037).

Conclusion:
Across three academic centers, patients with FST I-III demonstrated significantly greater clinical improvement on NB-UVB than patients with FST IV-VI at mid-year, year-end, and end of follow-up. Potential contributors include disease presentation differences, variability in dosing regimens, and post-inflammatory hyperpigmentation mimicking persistent disease in patients with skin of color, leading to perception of lesser improvement. Larger retrospective and prospective studies are needed to elucidate these disparities and inform treatment strategies to promote equitable outcomes.

A Multicenter Retrospective Study of Narrowband UVB Response Across Skin Types in Mycosis Fungoides

Background
Cutaneous T-cell Lymphoma (CTCL) is notorious for its ability to mimic benign dermatologic conditions. Thus, CTCL often has a delayed biopsy and diagnosis until months or even years down the line. This can increase baseline disease burden and worsen clinical outcomes. Previous studies have shown ranges of diagnostic delay from about two to six years for various types of CTCL, yet close to none explicitly stratify and analyze delay by Fitzpatrick skin types and subsequently explore possible disparities.
Methods
A single academic center CTCL database with a total of 266 patients with various types and stages of CTCL from 2004-2023 was retrospectively analyzed. Patients were excluded if pertinent study data was missing. Delay in diagnosis was calculated as months from patient-reported symptom onset to biopsy-proven diagnosis. Prolonged delay was pre-specified as greater than or equal to 2 years based on previous literature. Fitzpatrick skin type was dichotomized into types I-II and III-VI. Demographic, Mann-Whitney U (months delay vs Fitzpatrick binary), and χ2 analyses (prolonged delay vs advanced CTCL stage and prolonged delay vs systemic treatment) were performed on de-identified data using R Statistical Software (v4.5.1) via standard code, dplyr, and ggplot2 packages.
Results
Median diagnostic delay was 36 months (IQR 12-84) for 193 patients, and 61% experienced a diagnostic delay greater than 24 months. There was no statistically significant difference in diagnostic delay based on Fitzpatrick skin type (W=3193, p=0.79). About 19% were at least stage IIB, however, there was no association between prolonged delay and advanced stage at diagnosis (χ2=0.51, p=0.47). Additionally, there was no association between prolonged delay and receipt of systemic treatment (χ2=6.06, p=0.054).
Conclusion
CTCL maintained a median three-year diagnostic delay and no statistical shift in this delay across two sets of Fitzpatrick skin types. This reinforces CTCL’s clinical complexity, and underscores the need for larger, multi-center cohort studies that can verify if there is an association between diagnostic delay and higher Fitzpatrick skin type. In turn, this will help inform concrete early biopsy protocols to advance quality of care and health outcomes across Fitzpatrick skin types.

Multiyear Diagnostic Delay in Cutaneous T-cell Lymphoma: 2004-2023 U.S. Cohort Based on Fitzpatrick Skin Type

ABSTRACT:
INTRODUCTION
The increasing prevalence of metabolic diseases, such as non-alcoholic fatty liver disease
(NAFLD) and morbid obesity, has led to extensive research into the role of gut microbiota
and dietary factors in their development. This systematic review aims to synthesize current
evidence on how gut microbiome dysbiosis, and dietary patterns influence these conditions
and to evaluate potential therapeutic strategies. The gut microbiota, a diverse community of
microorganisms, plays a crucial role in regulating host metabolism and immune responses.
Disruptions in microbiota composition, referred to as dysbiosis, have been linked to the
development and progression of various metabolic disorders. This review examines the
intricate relationships between gut microbiota, metabolic health, and dietary influences to
identify potential intervention strategies.
METHODOLOGY
A comprehensive search was conducted across multiple databases to identify studies
investigating the impact of gut microbiota and diet on metabolic diseases. The review
includes longitudinal cohort studies, meta-analyses, and mechanistic research. Studies were
selected based on their focus on gut microbiota composition, dietary effects, and microbial
therapies in relation to NAFLD and obesity.
RESULTS AND DISCUSSION
Dysbiosis and impaired gut barrier function are closely associated with the progression of
metabolic-associated liver diseases and obesity. Microbial metabolites, such as short-chain
fatty acids (SCFAs), play significant roles in modulating liver metabolism and systemic
inflammation. Changes in gut microbiota composition over time correlate with variations in
metabolic parameters. Probiotic and prebiotic interventions demonstrate potential in
improving lipid profiles and insulin resistance.
CONCLUSION
Dietary interventions, probiotics, prebiotics, and emerging microbiota-targeted therapies have
shown promise in restoring gut microbiota balance and improving metabolic health.
However, the path forward requires addressing significant research gaps. These include the
need for large-scale, longitudinal studies to establish causal relationships between dietary-
induced microbiota changes and metabolic diseases, as well as exploring the roles of non-
bacterial components of the microbiota, such as fungi, viruses, and archaea.
Furthermore, personalized nutrition strategies that account for individual variability in
genetics, baseline microbiota composition, and lifestyle factors hold the potential to
revolutionize the prevention and treatment of metabolic diseases.

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Autophagy-Driven Modulation of HLA Class I in Coxsackievirus B Infected Human Pancreatic β-Cells

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