Faculty Bibliography

INTRODUCTION/BACKGROUND:The American Urological Association (AUA) Annual Meeting is consistently competitive, accepting approximately one-third of the scientific abstracts submitted. Following abstract presentation, manuscript publication offers the opportunity to more widely disseminate research findings and methodology. Several prior studies have evaluated the publication rate of urology abstracts presented at regional and/or national conferences. In this study, we aim to both identify factors of Pediatric Urology abstracts presented at the annual meeting that were associated with an increased likelihood of manuscript publication and evaluate trends over time. METHODS:All Pediatric Urology abstracts presented at AUA annual meetings from 2013 to 2022 were reviewed. Data was collected on primary author degree type, presentation format (e.g. poster v. podium), and author geographic region. Manuscripts were searched for on PubMed and Google Scholar using the abstract titles and authors' names. Journal name, year of publication, and journal impact factor were recorded for published manuscripts. Impact factors were based on 2024 published values. SPSS statistical software was then used to analyze descriptive statistics and perform chi square analysis for categorical variables. Descriptive statistics, chi-square tests with pairwise Bonferroni correction, Cochran-Armitage trend testing, multivariable logistic regression, and Kaplan-Meier time-to-event analyses were performed. RESULTS:604 Pediatric Urology abstracts were presented from 2013 to 2022. Of these, 456 (75.5%) were moderated posters, 112 (18.5%) were videos, and 36 (6.0%) were podium presentations. 240 (39.7%) of these resulted in published manuscripts. Median time to publication was 1 years (IQR 1-2). 88.8% of published manuscripts (n = 213) had a physician listed as first author. Though there was an upward trend in the number of abstracts presented at annual meetings from 2013 (n = 72) to 2022 (n = 94), the rate of manuscript publication did not differ significantly across years (p = 0.066). An ordinal trend test, however, indicated a modest decline in publication rate across the study period (Cochran-Armitage p = 0.030). Manuscripts were published in 55 different journals with a median impact factor of 2.3 (IQR 1.9-6.8). 217 manuscripts (90.4%) were published within two years of abstract presentation. In contrast to several prior studies which found that podium presentations were more likely to subsequently get published as manuscripts, moderated poster presentations demonstrated the highest publication rate (44.7%), followed by podium presentations (30.6%), and video presentations (22.3%). Pairwise comparison with Bonferroni correction showed this format effect was driven by the difference between moderated poster and video presentations (adjusted p < 0.001); podium presentation were not statistically separable from either group.AUA geographic region was not associated with likelihood of manuscript publication (p = 0.648). CONCLUSIONS:The overall manuscript publication rate for Pediatric Urology abstracts at the AUA annual meeting over ten years was 39.7% (publication searches conducted through March 2026). Presentation format was significantly associated with publication likelihood; pairwise comparison showed this effect was driven by the difference between poster and video presentations, while podium presentations were not statistically separable form either group given the limited window in which podium was offered (2019 and 2022). With moderated poster presentations demonstrating the highest publication rate. Geographic region did not impact likelihood of publication. The annual conversion rate showed a modest decline across the study period (trend p = 0.030), which may partly reflect shorter publication follow-up for recent meeting years.

UNLABELLED:Pelvic fractures result in prolonged pain and immobility. In a randomized controlled trial of patients with pelvic fracture, whether abaloparatide (ABL) vs. placebo (PBO) improves healing at 3 months was evaluated. There was no significant difference in CT radiologic healing, physical performance, or change in pain in ABL vs. placebo. PURPOSE/OBJECTIVE:To determine if abaloparatide (ABL) vs. placebo (PBO) improves radiologic healing, pain, and functional outcome at 3 months in patients with pelvic fracture. METHODS:Postmenopausal women and men ≥ 50 years old, enrolled within 4 weeks of pelvic fracture (n = 48), were randomized to blinded ABL vs. PBO. The primary endpoint, fracture healing at 3 months, was assessed by two radiologists using a 5-point scale for cortical bridging from CT images comparing groups by Jonckheere-Terpstra test. The odds of healing (3 or 4 cortices bridged) were analyzed with Mantel-Haenszel relative risks (RR). Pain was assessed monthly by Numeric Rating Scale (NRS). The Short Physical Performance Battery (SPPB; walk speed, chair stands, and balance) evaluated functional mobility. RESULTS:Groups were balanced with a mean age = 82, 93% were female, 98% had multiple rami fractures, 67% had sacral fracture, and 36% had ≥ 1 displaced fracture. CT images at 3 months showed no significant difference in bridging score distribution (indicator of healing) in patients with ABL vs. PBO (p = 0.15) after adjusting for age, sacral fracture, displacement, or compliance. When evaluating individual fractures (n = 81), similar bridging scores were seen with ABL and PBO (p = 0.13). When patients were stratified as healed or not healed, 39% were healed with ABL and 64% healed with PBO (RR 0.61; 95% CI 0.33, 1.12). When looking at the 81 individual fractures, 47% were healed with ABL and 53% healed with PBO (RR = 0.88; 95% CI 0.55, 1.40). Using least square means controlling for age, sacral, and displaced fracture, NRS pain score was higher in the placebo than the ABL group at baseline (p < 0.05), but there were no further group differences in change in pain score SPPB and TUG scores improved over time in both groups without group differences. CONCLUSION/CONCLUSIONS:In this small study, there was no significant difference in CT radiologic healing, physical performance, or change in pain with ABL vs. placebo in patients with acute pelvic fracture. TRIAL REGISTRATION/BACKGROUND:ClinicalTrials.gov identifier: NCT04249232 registered January 27, 2020.

Microglia perform the function of CNS macrophages and act as the primary immune cells in the brain. They surveil the environment, phagocytose cellular debris, maintain homeostasis and respond to tissue damage. While under physiological conditions they play a role in supporting neurons, activated microglia participate directly in the degeneration of neurons in the substantia nigra, as the hallmark of the Parkinsons disease (PD). Their detrimental effects result from direct phagocytosis of dopaminergic neurons as well as via neuroinflammation and release of toxic reactive oxygen and nitrogen species. This pathological shift is driven by a complex interplay of genetic predispositions, such as LRRK2 and GBA mutations, and environmental triggers like toxins and gut dysbiosis.A central mechanism of this neurodegeneration involves extracellular α-synuclein acting as a danger signal (DAMP), which activates microglial Toll-like receptors (e.g., TLR2) to initiate a severe inflammatory cascade. Furthermore, the extreme biophysical stability of aggregated α-synuclein overwhelms the microglial endolysosomal network, leading to lysosomal failure, "frustrated phagocytosis," and the active propagation of the disease via exosomal shedding. Relieving this maladaptive chronic neuroinflammation is a primary therapeutic goal. Modern strategies aim to break this vicious cycle through precise interventions like NLRP3 inflammasome inhibition and autophagy enhancement. Concurrently, advanced fluid biomarkers, such as seed amplification assays (SAA), alongside multidimensional neuroimaging techniques (PET, SPECT, MRI), are proving crucial for detecting these early microglial and pathological changes to guide personalized, disease-modifying therapies of PD.

IMPORTANCE/UNASSIGNED:Many patients are diagnosed with atypical lesions or lobular carcinoma in situ (LCIS); however, evidence- and consensus-based guidelines for the management of many of these lesions are limited. OBSERVATIONS/UNASSIGNED:The American Society of Breast Surgeons, in collaboration with the Society of Breast Imaging and College of American Pathology, assembled a steering group to create guidelines for the management of atypical lesions and LCIS, inclusive of flat epithelial atypia (FEA), atypical ductal hyperplasia (ADH), atypical lobular hyperplasia (ALH), classic LCIS (C-LCIS), and the variant LCIS forms pleomorphic LCIS (P-LCIS) and florid LCIS (F-LCIS). The natural history of ADH, ALH, and C-LCIS suggests that these lesions are associated with an elevated future breast cancer risk; therefore, patients diagnosed with these lesions should be recommended to undergo comprehensive risk assessment and counseling about breast cancer risk-reducing strategies. The magnitude of future breast cancer risk associated with P-LCIS and F-LCIS remains uncertain, yet if these lesions are determined to be hormone receptor positive, risk-reducing medications should be considered. There is no evidence that FEA is associated with an elevated future breast cancer risk. A second pathology review confirmation is recommended for ADH, should be considered for FEA, and is not necessary for ALH or LCIS. Currently available evidence supports the need to diagnostically excise most ADH, P-LCIS, and F-LCIS cases identified on core biopsy, although some ADH cases fulfilling strict criteria and multidisciplinary consensus can be observed. P-LCIS and F-LCIS require a negative margin, but ADH does not. ALH and C-LCIS can be safely observed if the core biopsy diagnosis is concordant with imaging features (ie, radiographic-pathologic concordance is established). Provided radiologic-pathologic concordance is confirmed, diagnostic excision is generally not indicated after a diagnosis of FEA alone. CONCLUSIONS AND RELEVANCE/UNASSIGNED:These guidelines provide evidence-informed, consensus-based recommendations for the management of atypical lesions of the breast, including ADH, ALH, FEA, C-LCIS, P-LCIS, and F-LCIS. Practicing clinicians who treat patients with atypical breast lesions or LCIS should consider integrating these guidelines into clinical management.

Sellar region neurocytoma (SELN) is a rare neoplasm whose relationship to other neurocytomas within the central nervous system (CNS) has remained unclear. Prior reports have variably classified SELN as a variant of extraventricular neurocytoma (EVN), while immunohistochemical and ultrastructural studies have suggested a hypothalamic origin. Here, we performed unsupervised clustering of DNA methylation data across a large pan-cancer reference set and identified SELN (n = 20) as distinct from other neurocytomas and regional mimics, as well as clustering with neuroendocrine tumors from other organ sites. SELN exhibited a CIMP-like phenotype, TTF1 negativity (0/8), and AVP (vasopressin) promoter hypomethylation, implicating a magnocellular hypothalamic cell of origin. In evaluable cases, a neuronal/neuroendocrine immunophenotype was observed (synaptophysin 8/8, chromogranin A 5/5) with absent pituitary transcription factor expression (PIT1 and TPIT negative 0/4). DNA sequencing (n = 5) and RNA-based fusion profiling (n = 4) did not detect recurrent mutations or gene fusions, respectively. Patients often presented with visual disturbances or headaches and spanned pediatric and older age groups (median 42 years, range 12.5-75), with no sex predilection. Despite locally aggressive imaging features in some cases (cavernous sinus invasion, carotid encasement, hydrocephalus), disease-free survival (n = 13) was comparable to central neurocytoma, with no disease-related deaths during the limited follow-up. Together, these findings support SELN as a molecularly distinct hypermethylated neuroendocrine-like epitype and clinicopathologic entity.

BACKGROUND:Tracheal intubation is a common yet high risk procedure in the critically ill with as many as half experiencing peri-intubation adverse outcomes. RESEARCH QUESTION/OBJECTIVE:We aimed to evaluate the comparative effectiveness and safety of various sedative agents used for endotracheal intubation of the critically ill patient in the emergency department, intensive care unit, operating room, and pre-hospital setting. STUDY DESIGN & METHODS/METHODS:We conducted a network meta-analysis and systematic review of randomized controlled trials. We searched MEDLINE, EMBASE, PubMed, Cochrane, and trial registries from inception to December 10, 2025 for Randomized controlled trials (RCTs) comparing two or more sedative agents in critically ill adults or children undergoing endotracheal intubation. Outcomes of interest were hemodynamic instability during intubation, hypoxemia, cardiac arrest, mortality, intensive care unit and hospital length of stay, vasopressor use, adrenal insufficiency, and first-pass success. Reviewers screened, extracted data, and assessed risk of bias using the Cochrane RoB 2 tool independently and in duplicate. We performed frequentist random-effects model network meta-analysis and used the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach to rate certainty in estimates. RESULTS:We included 21 RCTs enrolling 6,031 patients across Intensive Care Unit, Emergency Department, Operating Room, and pre-hospital settings. Compared with etomidate, there is probably more hemodynamic instability during intubation with ketamine (RR 1.31, 95% CI 1.15-1.48; moderate certainty). Ketamine-propofol may decrease hemodynamic instability during intubation compared with etomidate (RR 0.44, 95% CI 0.27-0.72; low certainty) and ketamine (RR 0.34, 95% CI 0.21-0.56; low certainty). Compared with etomidate, ketamine may decrease the need for the initiation of post-intubation continuous infusion vasopressors (RR 0.80, 95% CI 0.50-1.28; low certainty). Etomidate caused increased adrenal suppression compared with other agents. INTERPRETATION/CONCLUSIONS:When considering sedation agents for endotracheal intubation of the critically ill, etomidate probably causes less hemodynamic instability during intubation when compared with ketamine. However, etomidate may increase the need for the initiation of post-intubation continuous infusion vasopressors when compared with ketamine and increases adrenal suppression. The clinical importance of these competing effects remains uncertain. Ketamine-propofol may decrease hemodynamic instability during intubation when compared with etomidate and ketamine though the available evidence is too limited and uncertain to support firm conclusions and further randomized trials are needed.

Pathological deposition of endogenous material within tissues represents a central, unifying mechanism across a broad spectrum of prevalent human diseases. Atherosclerosis and Alzheimer's disease (AD) exemplify this paradigm: atherosclerosis is driven by subendothelial accumulation of apolipoprotein B-containing lipoproteins, cholesterol crystals, and hydroxyapatite, while AD is characterized by cerebral deposition of misfolded amyloid-β (Aβ) and/or hyperphosphorylated tau. Emerging evidence implicates substantial lipid dyshomeostasis in AD pathogenesis, including lipid-droplet-accumulating microglia and widespread lipidomic disruption, blurring the categorical boundary between "lipid" and "protein" deposition diseases. Apolipoprotein A-I (apoA-I) dysfunction bridges both domains: post-translational modifications and point mutations impair reverse cholesterol transport in atherosclerosis and simultaneously promote apoA-I amyloid fibril formation in systemic amyloidosis. Across atherosclerosis, AD, systemic amyloidoses, immune complex-mediated nephropathies, crystal arthropathies, and lysosomal storage disorders, shared pathophysiologic processes emerge: production-clearance imbalance, conformational transitions favoring aggregation or crystallization, microenvironmental modulation by extracellular matrix components, and chronic sterile inflammatory responses driven by NLRP3 inflammasome activation. In this review, we synthesize deposition biology using atherosclerosis and AD as primary paradigms, integrate mechanistic insights from related disorders, highlight convergent molecular pathways including NLRP3, proteostasis, and glymphatic clearance, and discuss diagnostic and therapeutic strategies. A conceptual framework unifying these conditions as variations on a common deposition theme is proposed to guide broadly applicable precision therapies.

BACKGROUND/UNASSIGNED:It is unknown how the increased range of motion and improved gait mechanics provided by total ankle arthroplasty (TAA) affects the progression of subtalar arthritis compared with ankle arthrodesis (AA). We hypothesized that patients treated with TAA would have a lower incidence of postoperative subtalar arthrodesis (SA) compared to AA. METHODS/UNASSIGNED: <.05. RESULTS/UNASSIGNED: > .05). In a multivariate analysis, AA remained associated with increased risk of requiring SA (OR = 1.90, CI = 1.01-3.56). CONCLUSION/UNASSIGNED:In this study, we found a significantly higher incidence of subtalar arthrodesis following AA compared with TAA. Surgeons may consider the risk of progression to SA when deciding between TAA and AA for patients with advanced ankle arthritis, particularly in preoperative counseling for patients without existing subtalar arthritis, as TAA may offer an opportunity to mitigate this risk. LEVEL OF EVIDENCE/UNASSIGNED:Level III, retrospective comparative study.