United States

Achondroplasia, the most prevalent skeletal dysplasia, is a genetic disorder caused by activating mutations in the FGFR3 gene impairing endochondral ossification of long bones. Clinical manifestations include disproportionate short stature and multisystem complications. Management has been limited to supportive care, surgical limb lengthening, and recombinant human growth hormone. The latter two carry significant risks and provide modest benefits, respectively. Recently, targeted molecular therapies have emerged as promising alternatives. This review highlights three investigational agents: Vosoritide, Infigratinib, and Naviperigride. Vosoritide, an injectable C-type natriuretic peptide analog, reduces MAPK pathway overactivation; Infigratinib, an oral FGFR1-3 inhibitor, directly suppresses downstream signaling; and Naviperigride, a long-acting CNP prodrug, sustains MAPK inhibition. Clinical trials in children aged 5 years and older demonstrate improved annualized growth velocity compared to baseline: 1.7 cm/year with Vosoritide, 6.0 cm/year with Infigratinib, and 5.4 cm/year with Naviperigride. Safety profiles are favorable with few to no significant treatment-related adverse events reported in the trials reviewed; radius fracture, adenoidal hypertrophy, and sleep apnea were reported for Vosoritide, injection site reactions were reported for Naviperigride, and nasopharyngitis was reported for Infigratinib. Direct comparisons across trials are limited, but available data suggest all three therapies bring growth trajectories of children with achondroplasia closer to unaffected peers. Long-term outcomes, particularly regarding comorbidities such as foramen magnum stenosis, spinal stenosis, and sleep apnea, remain under investigation. These emerging treatments represent a paradigm shift in achondroplasia management, underscoring the need for head-to-head studies and evaluation of combination strategies to optimize efficacy and durability. 


AMA Research Challenge 2025 

Achondroplasia Treatments in Children Aged 5 and Older

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AMA Research Challenge 2022

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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.

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

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
Recently there has been a greater pursuit in the field of orthopaedic research to understand psychological factors and their effect on surgical recovery. Despite the recent expansion in relevant research, we still do not fully understand which risk factors may contribute to the development of depression and anxiety following medial patellofemoral ligament reconstruction (MPFLR) or the impact of these psychological conditions on surgical outcomes. The purpose of this study is to quantify the prevalence of depression and anxiety and its influence prior to and following MPFLR.
Methods
Patients undergoing MPFLR between 12 and 65 years of age were identified using the Truven MarketScan Research Database. Using the International Classification of Diseases, Tenth Revision (ICD-10) codes, patients were screened for a depression or anxiety diagnosis up to three months prior to surgical intervention and up to one year following surgery. Patients were classified as having a preoperative, postoperative, or no depression or anxiety diagnosis. We compared opioid use, reoperation rates, and healthcare utilization costs based on sex and on psychological diagnosis.
Results
A total of 5,109 patients underwent MPFLR between April 2020 and December 2021, of which 3,007 were female (58.9%). Depression or anxiety claims were seen in 1,965 (38.5%) of patients. Preoperatively, 1,071 (35.6%) of females and 313 (14.9%) of males had a new diagnosis of depression or anxiety, and 817 (27.2%) of females and 558 (26.5%) of males used prescribed opioid medications. Postoperatively, 406 (13.5%) of females and 175 (8.3%) of males had a new psychological diagnosis, and 848 (28.2%) of females and 413 (19.6%) of males used opioids at least 60 days following surgery. The overall revision rate was 8.4% (293 females, 137 males). Patients with a new postoperative diagnosis of anxiety or depression had the highest rate of revision MPFL reconstruction (11.2%). During the three-month preoperative phase, the median cost of care for females and males was similar [$1,928 (IQR: $1,020-$3,623) vs. $1,932 ($1,011-$3,436)]. However, during twelve postoperative months, the median cost of healthcare utilization for females was notably larger than for males [$6,822 ($3,498-$13,401) vs. $4,767 ($2,391-$9,886)].
Conclusion
Our data shows that females and patients with depression or anxiety have poorer outcomes following MPFL reconstruction, specifically prolonged opioid use, higher revision rates, and greater healthcare utilization costs. We recommend the addition of targeted psychiatric rehabilitation for these vulnerable cohorts, which may prevent opioid use disorders, promote MPFL healing, and allow greater return to activity.

Prevalence of Depression and Anxiety Following MPFL Reconstruction for Recurrent Patellar Instability

Background
Pelvic incidence (PI) is an anatomical parameter determined by the bony morphology of the pelvis, foundational to determining sagittal spinal alignment. PI has been closely linked to compensatory mechanisms in spinal deformity and overall health-related quality of life. Both excessive and insufficient PI have been associated with adverse outcomes. Prior cross-sectional studies have shown minimal variation in PI during childhood and adolescence. However, our group has identified, through longitudinal analysis, a subset of pediatric patients who experience significant changes in PI over time. This study aimed to investigate the morphological basis for these changes. We hypothesized that changes in PI could result from alterations in the sacral endplate, changes in the orientation or shape of the bony pelvis, or rotation through the sacroiliac (SI) joints.
Methods
We conducted a retrospective study of pediatric patients who demonstrated a change in PI exceeding 6 degrees (in either direction) on lateral spine radiographs obtained at least one year apart. Patients were included only if all relevant bony landmarks were clearly visible on both radiographs. We defined three novel angular measurements to assess pelvic morphology:
• S1-S2 Angle - the angle between the S1 and S2 endplates, used to assess changes in sacral slope. 
• ASIS-PSIS-S1 Angle - the angle between a line connecting the anterior superior iliac spine (ASIS) and posterior superior iliac spine (PSIS) and a line extending to the S1 endplate. This angle was designed to evaluate SIJ rotation.
• Hip Angle - the angle formed between the PSIS-ASIS line and a line connecting the PSIS and femoral head center, measuring the vertical position of the hip center. 
Pearson correlation coefficients were calculated for each variable relative to change in PI.
Results
Of 75 patients initially identified, 34 met inclusion criteria. Change in the S1–S2 angle was positively correlated with change in PI (R = 0.56, p < 0.01). Change in hip angle was negatively correlated with PI (R = –0.38, p = 0.03). ASIS–PSIS–S1 angle showed no significant correlation (R = 0.04, p = 0.82).
Conclusion
Morphological measurements reflecting bony growth (sacral slope and hip center position) demonstrated significant correlation with changing PI, supporting the hypothesis that bony development drives PI changes in a subset of pediatric patients. There was no association between PI change and SIJ rotation. These findings underscore the importance of bony growth modulation as a potential future target in managing sagittal alignment during skeletal development.


Characterization of Changing Pelvic Incidence in Pediatric Patients: Identifying the Morphological Changes that Drive Alterations in Pelvic Incidence

Abstract Title:
Medical-Student Led Health Education Workshops for Justice-Involved Populations

Background:
Each year, over 600,000 individuals are released from incarceration in the U.S., many of whom experience high rates of physical and behavioral health conditions. For uninsured individuals, prison or jail may represent their only consistent contact with the healthcare system. Upon reentry, barriers such as low health literacy, housing insecurity, and employment challenges often interfere with chronic disease management. Prior studies suggest that health education interventions can reduce stigma, improve trust in the healthcare system, and enhance post-release engagement. Medical education literature has called for increased exposure to justice-involved populations to deepen student understanding of structural determinants of health. However, a systematic review shows that most medical students receive limited training in this area.

Methods:
To address this gap, we designed a medical student–led health education workshop series at the Middlesex County Juvenile Detention Center in New Jersey. The series covers four core topics: Mental Health, Healthy Relationships, Sexually Transmitted Infections (STIs), and Navigating the Healthcare System; each selected in collaboration with facility staff. Each one-hour, trauma-informed session incorporates videos, interactive activities, and guided discussion. Medical students serve as facilitators, using accessible language and avoiding technical jargon. No identifying information is collected from participants, and the program is framed as a service-learning and educational initiative. 

Results:
As student facilitators, we observed high levels of engagement among participants, including active discussion and thoughtful questions. Contrary to initial assumptions about potential disinterest, students demonstrated enthusiasm and curiosity throughout the sessions. Feedback from both staff and participants guided iterative improvements in communication strategies, emphasizing clarity and contextual understanding. Interactive discussions frequently revealed misconceptions and highlighted the impact of prior life experiences on participants’ perspectives. These insights informed our continued use of a non-assumptive, participant-centered approach.

Conclusion:
This workshop series serves as a dual-impact model to enhance medical student education while addressing health literacy among justice-involved youth. The program fosters early exposure to historically underserved populations, helping to cultivate more empathetic and justice-conscious future providers. We aim to sustain and expand this initiative as a recurring educational experience for both youth and medical students.

The Impact of Medical-Student Led Health Education Workshops for Justice-Involved Populations

Background: Testosterone deficiency in men is often framed as a biological or age-related condition, yet hormone levels may also reflect broader social determinants of health (SoDH) and masculinity-related stressors. As a hormone tied to male identity, testosterone may operate as both a physiological signal and a social barometer. This study applied the Healthy People 2030 SoDH framework, integrating economic stability, education, healthcare access, neighborhood environment, and social context with biological and behavioral factors, to examine predictors of testosterone deficiency in U.S. men.
Methods: We analyzed data from four NHANES cycles (2011–2016, 2021–2023), including 10,357 men aged ≥18 years with valid total testosterone measurements. Men reporting exogenous testosterone prescriptions (n = 41) were excluded. Testosterone deficiency was defined as total serum testosterone <300 ng/dL. Predictor variables included BMI, fasting glucose, sedentary time, sleep duration, depressive symptoms (PHQ-2 ≥3), smoking, income-to-poverty ratio, employment, education, health insurance, usual source of care, housing size, marital status, and race/ethnicity. Multivariable logistic regression models adjusted for age and NHANES survey design. All analyses were performed in R version 4.5.0
Results: The prevalence of testosterone deficiency was 25.7%, declining from 28.1% in 2011–2012 to 20.3% in 2021–2023 (p-trend <0.01). Obesity (BMI ≥30) (AOR = 2.69, 95% CI [2.36–3.06], p <0.001), impaired fasting glucose (100–125 mg/dL) (AOR = 1.55, 95% CI [1.27–1.90], p <0.001), diabetes-range glucose (≥126 mg/dL) (AOR = 2.92, 95% CI [2.03–4.21], p <0.001), and prolonged sedentary behavior (≥8 h/day) (AOR = 1.39, 95% CI [1.14–1.70], p <0.01) were independently associated with greater odds of deficiency. Men without a usual source of care had higher odds (AOR = 1.27, 95% CI [1.05–1.54], p <0.05). Current smoking was associated with lower odds (AOR = 0.79, 95% CI [0.65–0.97], p <0.05). In the social context domain, never-married men had significantly lower odds compared with married men (AOR = 0.70, 95% CI [0.57–0.86], p <0.001). Race/ethnicity, education, income, and employment were not significant predictors.
Conclusion: Testosterone deficiency in U.S. men is strongly shaped by metabolic and behavioral risk factors, but also by relational status and healthcare access. These findings support reframing testosterone as a biopsychosocial marker that reflects not only physiology but also the ways men inhabit social roles, relationships, and expectations of masculinity. Addressing men’s hormonal health may therefore require integrating medical care with broader attention to gendered norms, social stressors, and cultural context.

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