United States

Preeclampsia (PE) is a pregnancy-specific hypertensive disorder arising after 20 weeks of gestation and remains a major cause of maternal and neonatal morbidity. It originates from abnormal trophoblast invasion and inadequate spiral artery remodeling, leading to placental ischemia, endothelial dysfunction, and excessive mitochondrial reactive oxygen species (mitoROS). These events drive trophoblast injury, impaired angiogenesis, and systemic oxidative stress that not only compromise fetal development but also confer a two to four higher lifetime risk of cardiovascular disease and heart failure in 
affected women.

Conventional antioxidants have shown limited success, underscoring the need for targeted interventions. Mitochondria-directed therapeutics such as JP4-039, a nitroxide that scavenges mitoROS and stabilizes mitochondrial membrane potential, offer promise in restoring endothelial and placental health. We propose a placenta-targeted delivery systemusing CGKRK-engineered extracellular vesicles (EVs) loaded with JP4-039 to reduce oxidative injury, enhance vascular remodeling, and mitigate both acute placental dysfunction and long-term maternal cardiovascular risk in Preeclampsia.

AMA Research Challenge 2025 

JP4-039 as a Mitochondria-Directed Strategy to Address Cardiovascular
Dysfunction in Preeclampsia

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poster

Abstract Title: The Interface Between Host Microbiome and Common Medications 

Background: The human gut microbiome plays a critical role in drug metabolism, efficacy, and safety. While host genetics and comorbidities are known contributors to pharmacologic variability, emerging research highlights gut microbiota as a modifiable and underrecognized determinant. This narrative review synthesizes current evidence on bidirectional interactions between the gut microbiome and commonly prescribed medications in the U.S., including selective serotonin reuptake inhibitors (SSRIs), antihyperglycemics, ACE inhibitors, beta blockers, calcium channel blockers, Proton pump inhibitors (PPIs), and statins. 

Methods: A literature review was conducted using peer-reviewed primary research from PubMed and Google Scholar, limited to the past 20 years. Commonly prescribed medications were selected based on United States government’s Medical Expenditure Panel Survey (MEPS) data using the ClinCalc DrugStats database. The included drugs were fluoxetine, escitalopram, sertraline, duloxetine, quinapril, metoprolol, amlodipine, metformin, simvastatin, rosuvastatin, and esomeprazole. Eligible studies encompassed animal models, human interventional and observational studies, in vitro experiments, reviews, and meta-analyses. Non-peer-reviewed sources were excluded. 

Results: Studies show that antidepressants, particularly SSRIs such as fluoxetine and duloxetine, exhibit antimicrobial effects and reduce microbial diversity; meanwhile, gut bacteria like Streptococcus salivarius can bioaccumulate or inactivate these drugs, altering systemic concentrations and therapeutic responses. ACE inhibitors like quinapril are metabolized by Coprococcus comes, reducing oral bioavailability and potentially contributing to treatment-resistant hypertension, while also decreasing the abundance of pro-inflammatory microbes such as Klebsiella, which may support cardiometabolic health. Metformin improves glucose control partly by enriching beneficial microbes (e.g., Akkermansia, Butyricimonas); additionally, fecal microbiota transplantation from metformin-treated mice improves insulin sensitivity in humans. Beta blockers such as metoprolol undergo microbial metabolism that reduces drug bioavailability, while concurrently modulating microbial composition by increasing butyrate-producing taxa and decreasing pro-inflammatory species. Amlodipine is directly metabolized by gut microbes in fecalase models reducing drug availability; while also shifting microbial populations in ways that enhance gut barrier function. Statins influence bile acid metabolism and gut microbial profiles, contributing to their lipid-lowering effects; however, antibiotic-induced dysbiosis impairs statin efficacy in mice. PPIs reduce microbial diversity and increase pathogenic taxa such as Streptococcus, while the presence of Helicobacter pylori modulates PPI efficacy and associated risks. 

Conclusion: Drug-microbiome interactions are both class-specific and mechanistically diverse, involving microbial metabolism, drug bioaccumulation, immune modulation, and metabolic pathway shifts. These findings support a growing role for microbiome informed pharmacology and reinforce the need for further human studies to advance precision medicine and individualized treatment strategies.

The Interface Between Host Microbiome and Common Medications

Background
Chronic endometritis (CE) is defined by persistent inflammation of the endometrium, typically associated with microbial infections, including LPS-producing E. coli and Chlamydia. CE diagnosis occurs mainly in the setting of infertility. CE is commonly diagnosed by counting CD138+ plasma cells in stromal-dense areas of an endometrial biopsy. However, there is no standardized diagnostic criteria and plasma cells alone may be insufficient to reliably diagnose CE. Pathological diagnosis may be improved by measuring endometrial edema and increased endometrial stromal cell (eSC) density. Human eSCs express TLRs, including TLR4 and thus, are targets of LPS and other pathogen-associated molecular patterns (PAMPs). While previous studies identified increased eSC density and aberrant eSC functions in the setting of CE, these alterations have not been well-defined. In humans and the few species that menstruate, eSCs proliferate during the luteal phase and then eSCs decidualize (a differentiation process critical for implantation) during the mid-secretory phase. Our laboratory has pioneered the use of menstrual effluent (ME, shed endometrial tissue) for studying endometriosis. We hypothesize that infection-related alterations in eSCs will help better understand and diagnose CE.

Methods
Using ME collected from women (18-40 years) with no history of pelvic inflammatory disease, polycystic ovary syndrome, or endometriosis, eSCs were isolated and grown in culture media until confluency. Low passage ME-derived eSCs were treated with LPS (0-500 ng/ml) for 3 days and then analyzed for proliferation by CyQuant assay and decidualization potential by measuring the production of Insulin-like Growth Factor Binding Protein 1 (IGFBP1, a decidualization marker) by ELISA.

Results
Overall, proliferation assays revealed a significant increase in eSC numbers following LPS treatment compared to vehicle: 0 ng/ml vs. 25 ng/ml (p = 0.014), 0 ng/ml vs. 50 ng/ml (p < 0.0001), 0 ng/ml vs. 250 ng/ml (p = 0.0017). By contrast, decidualization assays revealed a significant decrease in IGFBP1 concentrations in LPS-treated conditions compared to vehicle: 0 ng/ml vs. 10 ng/ml (p = 0.0078), 0 ng/ml vs. 25 ng/ml (p = 0.0078).

Conclusion
LPS has opposing effects on eSC proliferation and decidualization. An increase in proliferation following LPS exposure supports the increased eSC density reported in the endometrium during CE and may promote endometrial polyp formation in confirmed CE cases. The decreased decidualization following LPS may contribute to the infertility observed in CE. Further research is needed to elucidate the potential mechanisms underlying these altered eSC phenotypes.

Defining the effects of chronic endometritis on the endometrium through menstrual effluent

Background: Rotator cuff repairs often fail due to insufficient biologic healing at the tendon-bone interface (enthesis). Patch augmentation has emerged as a promising strategy that promotes cellular infiltration, organized collagen deposition, and matrix remodeling. The objective of this review is to comprehensively evaluate the histologic and biochemical effects of scaffold augmentation, to compare the effectiveness of different augmentation materials, and to analyze commercially available implants with histologic evaluation in animals and human studies.

Methods: A PRISMA-guided search of PubMed, Scopus, and Embase through May 2025 identified forty-two eligible studies. Inclusion criteria were histologic and biochemical outcomes following rotator cuff repair with patch augmentation. Studies limited to biomechanical or imaging outcomes, in vitro or cadaveric models, reviews, editorials, technical notes were excluded. 

Results: Dermal matrix patches accelerated early neovascularization and collagen synthesis but often led to incomplete fibrocartilage formation and persistent type III collagen. ECM-derived patches showed progressive collagen alignment but were associated with inflammation. Synthetic polymers were successful at generating dense type 1 collagen with variable immune responses. Biologically augmented scaffolds demonstrated the highest collagen density and minimal macrophage infiltration. Demineralized bone matrix (DBM) achieved mature collagen crimp and fibrocartilage integration by eight weeks with low inflammation.

Among commercial products, REGENETEN, ArthroFLEX, and Dynagraft II demonstrated the most complete scaffold resorption and tendon-like remodeling. Conexa and Zimmer patches showed consistent integration, and Permacol and BioEnthesis exhibited limited improvements.

Conclusion: Patch augmentation enhanced healing following rotator cuff repair. Biologically augmented and DBM scaffolds yielded the most favorable histologic outcomes, followed by ECM-derived and synthetic patches. Dermal matrix patches showed strong early effects but lacked long-term integration. However, no definitive conclusions can be made due to the lack of high-quality human trials. These findings may guide scaffold selection and inform future design aimed at improving tendon-bone healing and reducing re-tear rates.

Rotator Cuff Patch Augmentation: Histologic Outcomes and Comparative Performance of Commercial Implants

Background
Industrial pollution has introduced toxic heavy metals—such as lead, mercury, and cadmium—into the environment, contributing to oxidative stress, DNA damage, and systemic health disorders. Marginalized and low-income communities of color are disproportionately affected due to proximity to industrial sites and legacy pollutants. Melanin, a biopolymer produced by melanocytes, is known for its protective role against ultraviolet radiation and oxidative damage. Emerging studies suggest that melanin may also function in heavy metal detoxification through binding and subsequent excretion via skin desquamation. However, the potential for melanin saturation and its consequences in chronically exposed individuals remain unclear.

Methods
A preliminary scoping review was conducted using PubMed with the search terms “melanin” and “heavy metal detoxification.” Fourteen peer-reviewed articles were identified and reviewed, with supplemental articles included via backward citation tracking and grey literature reviews. Articles were assessed for evidence of melanin-metal interactions, particularly the chelation capacity of eumelanin and pheomelanin. Emphasis was placed on mechanistic studies and environmental context, including disproportionate exposure among racially and socioeconomically marginalized communities.

Results
Experimental studies suggest that melanin binds various heavy metals—including lead, chromium, and arsenic—potentially reducing systemic toxicity. Eumelanin demonstrates higher metal-binding capacity than pheomelanin. Excretion via skin shedding may contribute to detoxification, though prolonged exposure could exceed melanin’s capacity, particularly in individuals with darker skin tones. Saturated melanin may lead to dermal bioaccumulation, localized oxidative stress, and chronic inflammation. Neuromelanin studies further support this metal-binding hypothesis, though translational human data are limited. Environmental racism and systemic inequities exacerbate exposure risks in communities of color, amplifying potential health burdens.

Conclusion
Melanin may play a dual role in detoxifying and accumulating heavy metals in the body. While protective at baseline, chronic exposure may shift melanin’s function toward a reservoir of toxicity, especially in individuals with greater melanin content and in communities facing environmental injustice. These findings underscore the need for further empirical research on melanin-metal interactions in humans and highlight the importance of addressing environmental and structural determinants of health in mitigating toxic exposures.


Melanin-Metal Interactions: A Double-Edged Shield in Environmental Toxicity and Health Disparities

Abstract Title: The Role of the Gut Microbiome in the Pathogenesis of Pre-Clinical Autoimmune Disease and the Prevention of Progression

Background: Autoimmune diseases often develop silently over years, with immune dysregulation and autoantibodies occurring long before symptoms appear. This silent period is what is referred to as “pre-clinical” autoimmunity. Pre-autoimmunity has been observed in several autoimmune diseases, including Rheumatoid Arthritis, Systemic Lupus Erythematosus, Sjögren’s Syndrome, Primary Biliary Cirrhosis, Inflammatory Bowel Disease, and Multiple Sclerosis. The gut microbiome has been increasingly implicated in this pre-clinical phase of autoimmune disease. This review examines how alterations in the gut microbiome can lead to the early stages of autoimmunity before symptoms begin and how the microbiome can be targeted to prevent the progression to autoimmune disease. 

Methods: The author carried out a literature review over PubMed using the keywords Gut microbiome pre-clinical autoimmune disease. 17 articles were reviewed. Peer-reviewed articles, systematic reviews, primary sources, clinical trials, case reports, cohort studies, interventional studies with appropriate control groups were included, while studies not related to pre-clinical autoimmunity, lacking control groups, in-vitro/ex vivo studies, and non-English publications were excluded. 

Results: A key factor in autoimmune disease pathology is gut dysbiosis, or alterations in the gut flora. This can cause increased gut permeability which allows bacterial byproducts like LPS to enter circulation triggering a cytokine cascade, altered gut-derived metabolites like changes in short chain fatty acids, tryptophan and bile acid metabolism leading to a pro-inflammatory state, and molecular mimicry which causes the immune system to attack self-tissues. Strategies to prevent the progression of pre-clinical autoimmunity to symptomatic autoimmunity include dietary intervention, supplementation of prebiotics and probiotics, fecal microbiota transplantation, microRNA therapies, targeted antibiotic therapy, autophagy regulation, and use of natural compounds. 

Conclusions: There is increasing recognition of the gut microbiome’s influence on immune system regulation and emerging evidence linking gut dysbiosis to immune dysregulation. Understanding how changes in the gut microbiome influence the expression of autoantibodies before the development of symptoms paves the way for mechanism-targeted, personalized interventions, and more accurate predictive and diagnostic tools, ultimately aiming to improve patient outcomes and potentially prevent the development of autoimmune disease. 


The Role of the Gut Microbiome in the Pathogenesis of Pre-Clinical Autoimmune Disease and the Prevention of Progression

Non-small cell lung cancer (NSCLC) presents a complex tumor microenvironment (TME) that modulates immune cell populations, including a distinct subset of SiglecF high neutrophils associated with tumor progression. While previous studies have identified soluble factors like cytokines as key modulators of immune cell behavior, the specific factors driving SiglecF high neutrophil induction in NSCLC remain unclear. We hypothesized that specific soluble factors within the NSCLC TME, particularly granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), and transforming growth factor-beta 1 (TGF-β1), synergistically induce the expansion of SiglecF high neutrophils, and that this induction would vary across different cancer models.

Flow cytometry was utilized to identify and quantify SiglecF high neutrophils across different cancer models, including KP NSCLC, B16-F10 melanoma, and 4T1 triple-negative breast cancer (TNBC) lines. Cytokine array analysis was conducted to determine the presence and levels of G-CSF, GM-CSF, and TGF-β1 in the TME of these models. ANOVA was used to assess the statistical significance of SiglecF neutrophil populations between the different models and in response to the presence of these cytokines. Statistical significance was defined as p < 0.05.

The KP NSCLC model demonstrated a significantly higher proportion of SiglecF high neutrophils compared to the B16-F10 and 4T1 models, which also had elevated levels compared to the naive control. Cytokine analysis revealed that GM-CSF and TGF-β1 were significantly elevated in the KP model compared to others, while G-CSF was highest in the 4T1 model. ANOVA analysis of in vitro cytokine induction indicated that GM-CSF and G-CSF synergistically induced SiglecF high neutrophils, with the highest induction observed when combined with TGF-β1.

The data suggest that the KP NSCLC TME uniquely promotes the induction of SiglecF high neutrophils, primarily through the synergistic effects of GM-CSF, G-CSF, and TGF-β1. These findings implicate these cytokines as key contributors to tumor progression via SiglecF high neutrophil induction, highlighting the potential for therapeutic targeting of these pathways in NSCLC. Future studies will focus on the inhibitory effects of SiglecF neutrophils on T-cell populations and explore strategies to mitigate their pro-tumoral functions. This research was supported by NIH P20GM135004 (Yan/Chesney) and the Summer Scholar Research Program.


Cytokine-Mediated Induction of SiglecF⁺ High Neutrophils in Non-Small Cell Lung Cancer Tumor Microenvironments

Abstract
Background: Arnold-Chiari malformation presents unique considerations during pregnancy and delivery due to its neurological implications. While cesarean delivery is often considered for safety, limited data exist regarding maternal outcomes across different racial groups and delivery methods in Chiari patients.

Objective: To assess maternal and obstetric outcomes by delivery method (vaginal vs. cesarean) in Black and White pregnant patients diagnosed with Chiari malformation.

Methods: A retrospective cohort study was conducted using TriNetX, an electronic health record-based research network. Separate cohorts of Black and White pregnant patients with Chiari malformation (ICD-10 Q07.0) were constructed. Patients were stratified by delivery method using CPT codes for vaginal and cesarean delivery. Maternal outcomes were compared using ICD-10 codes for gestational hypertension (O13), preeclampsia (O14), eclampsia (O15), perineal laceration (O70), and other labor-related complications (O60–O77).

Results: Among White patients (n=1,522), vaginal delivery was associated with a significantly lower risk of pre-eclampsia compared to cesarean delivery (4.0% vs 7.1%, p=0.02). This association was not statistically significant in Black patients (4.1% vs 5.7%, p=0.246). Although eclampsia was higher in vaginal deliveries for both races, it did not reach statistical significance. Perineal lacerations were significantly more common in vaginal deliveries among Black patients (12.7% vs 2.0%, p<0.001). No significant racial differences were found in rates of headache, fetal heart abnormalities, or hypertensive disorders.
Conclusion: 
White patients with AC malformation had significantly increased risk of pre-eclampsia following cesarean delivery, suggesting a potential benefit of vaginal delivery when feasible. Racial differences in maternal outcomes were limited but suggest potential disparities in delivery-related complications such as perineal trauma. Further studies adjusting for socioeconomic and clinical covariates are warranted.
Key words: Maternal outcomes; Chiari malformation; gestational hypertension, preeclampsia; eclampsia;
Declarations of interest: none
Funding: none


Beyond Assumptions: Racial and Delivery Method Outcomes in Pregnant Patients With Chiari Malformation

Introduction: The treatment of laryngeal cancer often results in alterations of speech and swallowing, which may contribute to the development of depression in this patient population and subsequently affect treatment outcomes and survivorship. This study aims to determine the prevalence of depression in patients with laryngeal cancer and identify contributing risk factors. 

Methods: Patients with laryngeal cancer were identified using ICD-10 codes within the TriNetX Research Network. Patients were stratified by treatment type (surgical versus non-surgical), age, socioeconomic (SES) risk factors, and post-treatment side effects. The effect of these factors on the development of depression was analyzed while controlling for cancer stage. 

Results: 93,018 patients with laryngeal cancer were identified. These patients had a significantly higher risk of depression compared to the overall head and neck cancer population (RR=1.15, 95% CI: [1.12,1.18]). Patients under 70 were more likely to develop depression than those over 70 (RR=1.27, 95% CI: [1.22,1.33]). SES risk factors were associated with over double the risk of depression (RR=2.67, 95% CI: [2.42,2.97]). Surgical treatment conferred a higher risk than non-surgical treatment modalities (RR=1.54, 95% CI: [1.41,1.68]). Patients who experienced long-term complications such as dysphagia, xerostomia, or malnutrition had a 7.62% increased risk of depression (p&lt;0.01). 

Conclusions: Patients with laryngeal cancer face a uniquely high risk of developing post-treatment depression. Future studies evaluating optimal screening protocols and supportive care strategies may help improve mental health care in this population.

Depression Among Patients With Laryngeal Cancer: A Retrospective TriNetX Study

Background
Developing novel, safe treatments for adolescent depression is imperative, as rates of depression are rising and conventional pharmacotherapies are often limited by modest efficacy and considerable side effects. Stanford Accelerated Intelligent Neuromodulation Therapy (SAINTTM), an optimized precision-targeted form of transcranial magnetic stimulation, is FDA-cleared for treatment-resistant depression in adults but remains understudied in adolescents. This pilot study investigates if SAINT, a rapid-acting noninvasive intervention with minimal side effects, can address this urgent need. We evaluate the safety, tolerability, and efficacy of SAINT in treatment-naïve adolescents experiencing their first episode of depression who remain antidepressant-free throughout treatment. By studying this demographic, we provide compelling evidence for SAINT as a first-line treatment. SAINT, however, requires a substantial time commitment—5 consecutive 10-hour days. This study introduces Truncated SAINT: a half-dose protocol of five consecutive 5-hour days supported by SAINT trials showing depression remission in highly treatment-resistant subjects after an average of 26 sessions. We hypothesize Truncated SAINT will yield equivalent antidepressant effects to Standard SAINT, with greater acceptability, preference, convenience, and overall satisfaction.

Methods
Two study arms will recruit 20 participants each to receive Standard or Truncated SAINT in a single-blind open-label design. The primary outcome is change in Children’s Depression Rating Scale-Revised (CDRS-R) scores one month post-treatment. Pre- and post-treatment interviews with adolescents and their parents provide measures of acceptability, preference, convenience, and satisfaction. All participants receive a brain resting-state functional magnetic resonance image (rs-fMRI) before treatment to identify the personalized treatment target. Two additional brain rs-fMRIs are obtained at the immediate and one-month follow-up visits to investigate changes in functional connectivity from baseline. Participants remain antidepressant-free for one month post-treatment, after which they resume standard psychiatric care. Participants are followed for 6 months to assess treatment durability.

Results
As of this writing, four participants have completed treatment for the study with three completing the primary outcome measure CDRS-R at the one-month follow-up. No adverse events have been reported. CDRS-R decreased from 60 to 22, 36 to 17, and 49 to 21 from baseline to one-month post-treatment in these subjects. 

Conclusion
Preliminary results suggest that both Standard and Truncated SAINT are safe and efficacious with no adverse events reported. Both participants who completed their one-month follow-up achieved depression remission. We expect SAINT to continue to demonstrate safety and efficacy and ultimately be considered as a first-line treatment for adolescent depression.


Investigating a Truncated Version of SAINT in Treatment-Naive Adolescents with Depression: An Open-Label Acceptability Trial.

Background
Cardiac myxomas are rare, benign tumors and the most common primary cardiac neoplasms. They are typically found in the left atrium and may present with nonspecific symptoms related to obstruction, embolization, or systemic effects. These tumors can be life-threatening if not detected and treated promptly. Because of their subtle and varied presentation, they can be overlooked until symptoms become severe. Cardiac imaging, such as transthoracic or transesophageal echocardiogram (TTE/TEE) is essential to accurate diagnosis. While traditional management involves open thoracotomy, video-assisted thoracoscopic surgery (VATS) has emerged as a less invasive alternative in select cases. Close follow-up with cardiology is important for management of supraventricular arrythmias that may occur after surgery. 

Case Presentation
A 49-year-old woman with no significant past medical history began experiencing dizziness, fatigue, chest discomfort, and near-syncopal episodes over a two-month period, worse with her typical exercise and running patterns. Initial neurologic evaluation, including brain MRI, showed a small colloid cyst and nonspecific left parietal findings but no clear explanation for her symptoms. An initial cardiac evaluation, which did not include imaging, was unremarkable and reassurance was given. After persistent symptoms, her primary care provider ordered a TTE, which revealed a large, mobile mass measuring 6.3 x 3.6 cm nearly filling the left atrium and prolapsing into the left ventricle, suspicious for a myxoma. She was urgently referred and underwent coronary angiography, which showed normal vessels and incidental blood flow to the mass. The patient quickly proceeded to surgical resection of the mass via thoracotomy. Pathology confirmed a left atrial myxoma measuring 6.2 x 5.5 x 2.5 cm. Postoperatively, she developed symptomatic atrial flutter with rates >200 bpm, thought to have stemmed from the right atriotomy during surgery. It was initially managed with TEE-guided cardioversion and ultimately resolved with catheter ablation. She has since returned to sinus rhythm and normal activity.
Discussion
This case highlights how cardiac myxomas can present with vague, nonspecific symptoms and mimic neurologic conditions, leading to delays in diagnosis. In this patient, echocardiography was critical in identifying the underlying cause of her symptoms. Prompt surgical resection prevented potential complications such as embolism or sudden cardiac death. The patient’s postoperative atrial arrhythmias underscore the importance of ongoing cardiac monitoring and follow-up. Clinicians should consider cardiac etiologies in patients with unexplained presyncope or exertional symptoms, especially when neurologic workup is inconclusive. Early detection and multidisciplinary care can lead to excellent outcomes in cases like this.


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