Citations

Abstract Health and biomedical science-related academic societies have played significant roles in the development and evolution of science and medicine, as well as the evolution of disciplines, including the diversification of medicine into specialties and subspecialties. They have also had formative roles in the development of clinical practice, professionalism, and training standards. The communities they establish promote knowledge creation and dissemination, provide career and professional development opportunities, articulate professional matters, offer networking opportunities, provide recognition, support members, and perform public engagement and advocacy work. They also play increasingly important roles in educating the public and disseminating objective, evidence-based medical and scientific information. Academic societies face challenges related to membership (recruiting new members and engaging and retaining current members), technology, hosting meetings and conferences, generational shifts (e.g., in demographics and attitudes toward working conditions, career paths, work-life integration), costs and logistics related to operations, and morale within institutions and professions. The Council of Faculty and Academic Societies of the Association of American Medical Colleges plays a unique role in supporting academic medical and related societies by providing an interprofessional forum for their interaction and dialogue, and is a vehicle for asserting their collective voice. To the extent that past is prologue, future advances in health care and science will depend, in part, on the resilience of academic societies and on the health professional workforces that they nourish.

Abstract Background Immigrant women experience disproportionate psychosocial stress driven by acculturation, socioeconomic hardship, discrimination, and transnational responsibilities. Despite evidence supporting culturally tailored stress‑management interventions, limited formative research has examined program preferences across diverse immigrant communities. Methods Using a community‑based participatory research (CBPR) approach, we conducted three language‑concordant focus groups (Somali, Spanish, English; n = 18) and a mixed‑methods survey (n = 88) with immigrant women in southeast Minnesota. Qualitative data were analyzed using constant comparative methods; quantitative data were summarized descriptively. Results Participants described intersecting stressors including caregiving burdens, financial insecurity, immigration‑related fears, bicultural identity strain, and transnational obligations (e.g., “Every day you are being told of problems back at home”). Barriers to discussing stress included stigma, limited culturally concordant care, religious norms discouraging emotional disclosure, and structural constraints such as lack of insurance (e.g., “How are you gonna pay for a therapist if you don't have health insurance?”). Coping strategies varied culturally but consistently emphasized social support, spirituality, and practical stress‑reduction techniques. Survey findings indicated strong preference for education on stress, stigma reduction, culturally and linguistically aligned support groups, and flexible delivery formats (in‑person, hybrid). Conclusions Immigrant women experience multifaceted stress shaped by minority stress processes and structural inequities. Findings highlight the need for culturally responsive, community‑informed stress‑management interventions that integrate education, social support, and flexible delivery modalities. These results directly inform adaptation of a stress‑management program for Somali, Spanish‑, and English‑speaking immigrant women.

ABSTRACT Extracellular vesicles (EVs) are increasingly recognized as mediators of intercellular communication in cancer. We previously demonstrated that re‐expression of the leucine‐rich domain (LRD) of neurofibromin (NF1) suppresses glioblastoma (GBM) invasion and limits microglia/macrophage infiltration into the tumor microenvironment (TME). Given the central role of tumor‐associated microglia/macrophages (TAMs) in GBM progression, we investigated whether NF1‐LRD‐containing EVs (NF1‐LRD‐EVs) could modulate TAM function and remodel the TME. Our results showed that NF1‐LRD‐EVs attenuated microglia and macrophage recruitment in migration assays, consistent with reduced microglia/macrophage recruitment observed in vivo . In parallel, treatment with NF1‐LRD‐EVs enhanced phagocytic activity of both microglia and iPSC‐derived macrophages, accompanied by induction of pro‐inflammatory cytokines TNF‐α, IL‐6, and IL‐1β, and downregulation of immunosuppressive mediators such as Arginase‐1 and IL‐10. Mechanistically, NF1‐LRD‐EVs induced ADAM17‐associated inflammatory signaling, accompanied by NF‐κB activation. Pharmacological inhibition of ADAM17 reduced TNF‐α release and attenuated NF‐κB activation, supporting a role for ADAM17‐dependent signaling in amplifying this inflammatory response. Together, these findings show that NF1‐LRD‐EVs reprogram TAMs toward a pro‐inflammatory phenotype and modulate the GBM immune microenvironment. These results provide a framework for understanding NF1‐LRD‐EV‐mediated immune regulation and support further investigation of EV‐mediated immune modulation of the TME.

Artificial intelligence (AI)–based protein structure prediction has rapidly entered nephrology, providing plausible atomic models for channels, transporters, receptors and scaffolds that previously lacked structural information. AlphaFold and RoseTTAFold now underpin mechanistic interpretations of inherited kidney diseases, including autosomal-dominant polycystic kidney disease, cystinosis and Alport syndrome, and support experimental design in cryo-electron microscopy and cryo-electron tomography. For nephrologists, this means that renal proteins no longer need to be treated as black boxes: genetic, biochemical and physiological data can now be mapped onto concrete three-dimensional scaffolds. However, the apparent precision of AI models can be misleading. Renal proteins frequently fall within underrepresented classes, including multipass membrane proteins, intrinsically disordered scaffolds, and human-specific isoforms with shallow multiple sequence alignments, where confidence scores may not accurately reflect model reliability. Current predictors typically deliver static snapshots, whereas transporters, channels and slit-diaphragm complexes function as dynamic ensembles embedded in specific lipid and macromolecular environments. Attempts to use AlphaFold directly for variant classification or to estimate changes in thermodynamic stability or function show only modest agreement with mutagenesis data, particularly for gain-of-function and dominant-negative alleles that depend on subtle conformational and interaction changes. Common pitfalls include overinterpreting oligomeric stoichiometry inferred from AlphaFold Multimer, reading too much into domain orientations with high predicted aligned error, and dismissing low-confidence regions as modelling failures rather than recognising intrinsically disordered, potentially regulatory segments. Integrative approaches combining cryo-electron tomography, crosslinking mass spectrometry and molecular dynamics can mitigate these limitations but remain labour-intensive and low-throughput. An explainable, hypothesis-driven use of AI that treats predicted structures as working scaffolds to be cross-validated against imaging, biophysics and functional assays offers the most reliable path towards a genuinely mechanistic nephrology and responsible clinical translation of AI-based structural insights.

Since October 2019, screening for methylmalonic acidemia (MMA) has been implemented in the Dutch Newborn Screening (NBS) program. Since implementation, most referrals for MMA have been the result of (maternal) vitamin B12 deficiency. Although vitamin B12 deficiency is an important condition and early detection can confer health benefits, its identification was not the original objective of the screening. We therefore examined whether genetic forms of MMA can be distinguished from acquired forms. Early distinction between these forms is essential for guiding clinical management, informing prognosis, and enabling appropriate genetic counseling. Specifically, we tested whether the use of Collaborative Laboratory Integrated Reports (CLIR) to complement NBS results improved specificity of the test for genetic MMAs. We found that with the use of CLIR, genetic conditions including methylmalonyl-CoA mutase (mut) deficiency and cobalamin (cbl) A, B, C and D deficiency can be partially differentiated from acquired causes. This results in a significant reduction in the number of second-tier tests required. However, this approach may also exclude certain other genetic causes. Based on all findings, we provide considerations and implications for MMA screening that may inform decision-makers in (other) NBS programs.

Background: Telogen effluvium (TE) is one of the most common forms of nonscarring alopecia. TE typically presents as sudden diffuse shedding of hair, and generally occurs 3–4 months after a triggering event such as physiological or psychological stress, certain medications, or hormonal changes. Despite the high prevalence of TE, no standardized clinical guidelines for the management of this condition currently exist. Objective: To address the lack of standard clinical guidelines for the management of TE, a multidisciplinary panel of dermatologists, dermatology advanced practice providers, and primary care providers convened to evaluate current evidence related to the treatment of TE. Methods: The primary research team, composed of 13 individuals, completed a comprehensive literature review of TE treatment. Then an expert panel conducted 2 rounds of article review, assessing each article based on the Strength of Recommendation Taxonomy (SORT) criteria and formulating consensus statements based on this data. An expert panel of 20 clinicians then evaluated the statements utilizing a structured eDelphi consensus process. Results: A total of 18 consensus statements regarding treatment recommendations for TE were reviewed by the expert panel. Of these, 3 statements addressed acute TE, while 15 focused on chronic TE. The panel evaluated each statement through open forum discussion, followed by voting and modification using the eDelphi methodology. Ultimately, 16 statements reached consensus following 2 rounds of the eDelphi survey. Conclusion: The self-limiting nature of acute TE warrants patient education, but no specific therapies were found to improve outcomes compared with placebo. While there is a gap in quality research regarding chronic TE treatment, current evidence suggests that topical minoxidil, vitamin D supplementation, and platelet-rich plasma may provide benefit in chronic TE based on individual clinical judgement.

Age-associated mitochondrial decline reduces NAD+ availability, impairs oxidative phosphorylation (OXPHOS), and leads to accumulation of reactive oxygen species (ROS) thereby reshaping cellular metabolism. However, the regulatory logic coupling mitochondrial aging to metabolic dysregulation resulting in tumorigenic cell-fate transitions has not been modeled systematically. In this work, we propose a Boolean biomolecular network model of mitochondrial aging and integrate it with metabolic, cell-cycle, and apoptotic biomolecular networks comprising 94 nodes and 370 edges. We then examined how NAD+ decline, hypoxia and extracellular ROS shifts the balance between OXPHOS and glycolysis. To this end, the consolidated network model underwent dynamical analysis to elucidate the system-level outcomes as well as its molecular triggers. In particular, we investigated whether the metabolic phenotypes are reversible and how cancer-driver perturbations act in the absence of extracellular pyruvate. The model recapitulates a quiescent, OXPHOS-leaning baseline and predicts that progressive NAD+ decline lowers OXPHOS propensity (0.686 to 0.186) while raising glycolysis (0.256 to 0.426). Hypoxia and extracellular ROS synergize glycolytic and hybrid oxidative–glycolytic (W/O) states. Furthermore, these two triggers, together with elevated mitogenic signaling, give rise to a hyperproliferative, glycolytic, and apoptosis-resistant cellular state. Interesting, this state is conditionally reversible wherein receptor tyrosine kinase (RTK) inhibition redirects this cell fate toward apoptosis and collapses the W/O state. Cancer-driver analysis further indicates that, without extracellular pyruvate, VHL loss and RAS, PI3K, or AKT activation preferentially stabilizes glycolytic and hybrid states. Age-resolved TCGA-BRCA analysis provided expression-level support for the predicted remodeling, with declining OXPHOS-associated expression and concurrent OXPHOS/glycolysis activity in older Basal-like tumors. Together, our results show that mitochondrial aging is a priming condition whose tumor-permissive metabolic output is gated by microenvironmental and nutrient inputs. The model provides a novel framework for evaluating age-associated metabolic reprogramming and predicting early tumorigenic cell fates.

Background: Dancers are at risk of femoroacetabular impingement (FAI) owing to supraphysiologic range of motion and associated demands placed on their hips. There remains a paucity of literature on midterm outcomes in dancers who undergo primary arthroscopy and labral repair for FAI. Purpose: To determine the rate of return to dance and patient-reported outcome measures in competitive dancers after hip arthroscopy with labral repair for FAI with minimum 2-year follow-up. Study Design: Case series; Level of evidence, 4. Methods: This study included dancers with FAI undergoing primary hip arthroscopy with labral repair from 2010 to 2022. Patient-reported outcome measures were collected at 2-year minimum follow-up: modified Harris Hip Score (overall, activities of daily living, gait, pain), Hip Outcome Score (activities of daily living, sports-specific subscale), Tegner Activity Scale, visual analog scale for pain, and surgery satisfaction. Patients were evaluated for preoperative radiographic measurements, postoperative return to sport, and revision surgery. Return to dance was evaluated. Results: Thirty-seven dancers were followed for a mean 7.4 years (range, 3.2-12.2) postoperatively (36 female and 1 male; mean ± SD age, 21 ± 7 years; mean body mass index, 23.3 ± 4.5). All outcome scores significantly improved postoperatively as compared with preoperatively ( P ≤ .037). Twenty dancers (71%) returned to dance. Of those who returned to dance, 17 (85%) returned to sport at the same or higher level as compared with the preoperative level. At final follow-up, 45% of dancers who initially returned to dance continued to dance. Of the dancers who no longer participated in dance at final follow-up, 7 (65%) quit dancing for nonhip-related reasons. Mean surgery satisfaction (0-10) at final follow-up was 7.1. Four patients (10%) underwent revision hip arthroscopy with revision labral repair. Conclusion: Hip arthroscopy with labral repair in dancers results in sustained improvements in function and pain at minimum 2-year follow-up. Most dancers return to their prior levels of dance, and nearly half remain active several years later. Notably, discontinuation of dance was often unrelated to hip symptoms, underscoring the importance of counseling patients on clinical and lifestyle factors influencing return to sport.