tbuckley/cabot-search huggingface dataset:
Disease severity and pruritus treatment outcomes in prurigo nodularis: A systematic review of randomized-controlled trials
Authors: Ryan S Q Geng, Siddhartha Sood, Jihad Waked, Rayyan Mahmood, Khalad Maliyar, Muskaan Sachdeva, Abrahim Abduelmula, Jensen Yeung, Asfandyar Mufti
Journal: Journal of the American Academy of Dermatology (2025)
The effect of respiratory motion compensation in intracardiac 4D flow magnetic resonance imaging on left ventricular flow dynamics, multicomponent particle tracing, and valve tracking
Authors: Paul R Roos, Thomas in de Braekt, Hildo J Lamb, Jos J M Westenberg
Journal:  (2025)

Abstract Aims 4D flow magnetic resonance imaging (MRI) has enabled evaluation of intracardiac flow dynamics by particle tracing for visualizing and quantifying complex flow patterns. The aim of this study was to assess the impact of respiratory motion compensation on 4D flow MRI–based left ventricular four-component particle tracing, valve tracking, and haemodynamics. Methods and results In this prospective cohort study, 4D flow MRI with and without respiratory motion compensation was performed in 15 healthy volunteers. Intracardiac particle tracing considered four components: direct flow, delayed ejection flow (DEF), retained inflow (RI), and residual volume. Data quality was assessed by comparing DEF and RI components. Particle tracing, valve tracking, kinetic energy (KE), and vorticity were compared between scan methods. Paired sample t-tests and intraclass correlation analysis were performed with an alpha of 0.05. DEF, RI, ejection fraction, and stroke volume were different between scan methods. Five participants showed DEF-RI mismatch &amp;gt; 10%. After excluding these, differences in flow fractions were non-significant. Differences in stroke volume, ejection fraction, and valvular flow mismatch between scan methods remained. Valve tracking was comparable between scan methods and correlated well with particle tracing. Absolute mismatch between particle tracing– and valve tracking–based mitral flow, and KE and vorticity at A-peak, was higher for non-compensated MRI. Conclusion Respiratory motion compensation can improve accuracy of intracardiac particle tracing based on 4D flow MRI by decreasing mismatch to retrospective valve tracking. For intracardiac particle tracing, respiratory motion compensation is advised. Robust data quality assessment for particle tracing–based analyses is equally crucial.
Selection for somatic escape variants in SERPINA1 in the liver of patients with alpha-1 antitrypsin deficiency
Authors: Natalia Brzozowska, Lily Y. D. Wu, Vera Khodzhaeva, William J. Griffiths, Adam Duckworth, Hyunchul Jung, Tim H. H. Coorens, Yvette Hooks, Joseph E. Chambers, Peter J. Campbell, Stefan J. Marciniak, Matthew Hoare
Journal: Nature Genetics (2025)

Abstract Somatic variants accumulate in non-malignant tissues with age. Functional variants, leading to clonal advantage of hepatocytes, accumulate in the liver of patients with acquired chronic liver disease (CLD). Whether somatic variants are common to CLD from differing etiologies is unknown. We analyzed liver somatic variants in patients with genetic CLD from alpha-1 antitrypsin (A1AT) deficiency or hemochromatosis. We show that somatic variants in SERPINA1 , the gene encoding A1AT, are strongly selected for in A1AT deficiency, with evidence of convergent evolution. Acquired SERPINA1 variants are clustered at the carboxyl terminus of A1AT, leading to truncation. In vitro and in vivo, C-terminal truncation variants reduce disease-associated Z-A1AT polymer accumulation and disruption of the endoplasmic reticulum, supporting the C-terminal domain swap mechanism. Therefore, somatic escape variants from a deleterious germline variant are selected for in A1AT deficiency, suggesting that functional somatic variants are disease-specific in CLD and point to disease-associated mechanisms.
Dopamine in the tail of the striatum facilitates avoidance in threat–reward conflicts
Authors: Iku Tsutsui-Kimura, Zhiyu Melissa Tian, Ryunosuke Amo, Yizhou Zhuo, Yulong Li, Malcolm G. Campbell, Naoshige Uchida, Mitsuko Watabe-Uchida
Journal: Nature Neuroscience (2025)

Responding appropriately to potential threats before they materialize is critical to avoiding disastrous outcomes. Here we examine how threat-coping behavior is regulated by the tail of the striatum (TS) and its dopamine input. Mice were presented with a potential threat (a moving object) while pursuing rewards. Initially, the mice failed to obtain rewards but gradually improved in later trials. We found that dopamine in TS promoted avoidance of the threat, even at the expense of reward acquisition. Furthermore, the activity of dopamine D1 receptor-expressing neurons promoted threat avoidance and prediction. In contrast, D2 neurons suppressed threat avoidance and facilitated overcoming the potential threat. Dopamine axon activation in TS not only potentiated the responses of dopamine D1 receptor-expressing neurons to novel sensory stimuli but also boosted them acutely. These results demonstrate that an opponent interaction of D1 and D2 neurons in the TS, modulated by dopamine, dynamically regulates avoidance and overcoming potential threats. During foraging with threat–reward conflicts in mice, dopamine modulates two competing neuron types in the striatum for flexible threat coping, from initial threat avoidance to eventual overcoming of the threat.
Subcellular proteomics and iPSC modeling uncover reversible mechanisms of axonal pathology in Alzheimer’s disease
Authors: Yifei Cai, Jean Kanyo, Rashaun Wilson, Shveta Bathla, Pablo Leal Cardozo, Lei Tong, Shanshan Qin, Lukas A. Fuentes, Iguaracy Pinheiro-de-Sousa, Tram Huynh, Liyuan Sun, Mohammad Shahid Mansuri, Zichen Tian, Hao-Ran Gan, Amber Braker, Hoang Kim Trinh, Anita Huttner, TuKiet T. Lam, Evangelia Petsalaki, Kristen J. Brennand, Angus C. Nairn, Jaime Grutzendler
Journal: Nature Aging (2025)

Dystrophic neurites (also termed axonal spheroids) are found around amyloid deposits in Alzheimer's disease (AD), where they impair axonal electrical conduction, disrupt neural circuits and correlate with AD severity. Despite their importance, the mechanisms underlying spheroid formation remain incompletely understood. To address this, we developed a proximity labeling approach to uncover the proteome of spheroids in human postmortem and mouse brains. Additionally, we established a human induced pluripotent stem cell (iPSC)-derived AD model enabling mechanistic investigation and optical electrophysiology. These complementary approaches revealed the subcellular molecular architecture of spheroids and identified abnormalities in key biological processes, including protein turnover, cytoskeleton dynamics and lipid transport. Notably, the PI3K/AKT/mTOR pathway, which regulates these processes, was activated in spheroids. Furthermore, phosphorylated mTOR levels in spheroids correlated with AD severity in humans. Notably, mTOR inhibition in iPSC-derived neurons and mice ameliorated spheroid pathology. Altogether, our study provides a multidisciplinary toolkit for investigating mechanisms and therapeutic targets for axonal pathology in neurodegeneration. Axonal spheroids disrupt neural circuits in Alzheimer's disease. In this study, using subcellular proximity labeling proteomics in human brain and iPSC modeling, the authors link spheroid formation to dysregulated mTOR, cytoskeletal and lipid transport signaling.
A functional single-cell metabolic survey identifies Elovl1 as a target to enhance CD8+ T cell fitness in solid tumours
Authors: Samantha Pretto, Qian Yu, Pierre Bourdely, Sarah Trusso Cafarello, Heleen H. Van Acker, Joren Verelst, Elena Richiardone, Lotte Vanheer, Amir Roshanzadeh, Franziska Schneppenheim, Charlotte Cresens, Maria Livia Sassano, Jonas Dehairs, Martin Carion, Shehab Ismail, Patrizia Agostinis, Susana Rocha, Tobias Bald, Johan Swinnen, Cyril Corbet, Sophia Y. Lunt, Bernard Thienpont, Mario Di Matteo, Massimiliano Mazzone
Journal: Nature Metabolism (2025)

Abstract Reprogramming T cell metabolism can improve intratumoural fitness. By performing a CRISPR/Cas9 metabolic survey in CD8 + T cells, we identified 83 targets and we applied single-cell RNA sequencing to disclose transcriptome changes associated with each metabolic perturbation in the context of pancreatic cancer. This revealed elongation of very long-chain fatty acids protein 1 ( Elovl1 ) as a metabolic target to sustain effector functions and memory phenotypes in CD8 + T cells. Accordingly, Elovl1 inactivation in adoptively transferred T cells combined with anti-PD-1 showed therapeutic efficacy in resistant pancreatic and melanoma tumours. The accumulation of saturated long-chain fatty acids in Elovl1 -deficient T cells destabilized INSIG1, leading to SREBP2 activation, increased plasma membrane cholesterol and stronger T cell receptor signalling. Elovl1 -deficient T cells increased mitochondrial fitness and fatty acid oxidation, thus withstanding the metabolic stress imposed by the tumour microenvironment. Finally, ELOVL1 in CD8 + T cells correlated with anti-PD-1 response in patients with melanoma. Altogether, Elovl1 targeting synergizes with anti-PD-1 to promote effective T cell responses.
Constructing future behavior in the hippocampal formation through composition and replay
Authors: Jacob J. W. Bakermans, Joseph Warren, James C. R. Whittington, Timothy E. J. Behrens
Journal: Nature Neuroscience (2025)

Abstract The hippocampus is critical for memory, imagination and constructive reasoning. Recent models have suggested that its neuronal responses can be well explained by state spaces that model the transitions between experiences. Here we use simulations and hippocampal recordings to reconcile these views. We show that if state spaces are constructed compositionally from existing building blocks, or primitives, hippocampal responses can be interpreted as compositional memories, binding these primitives together. Critically, this enables agents to behave optimally in new environments with no new learning, inferring behavior directly from the composition. We predict a role for hippocampal replay in building and consolidating these compositional memories. We test these predictions in two datasets by showing that replay events from newly discovered landmarks induce and strengthen new remote firing fields. When the landmark is moved, replay builds a new firing field at the same vector to the new location. Together, these findings provide a framework for reasoning about compositional memories and demonstrate that such memories are formed in hippocampal replay.
What makes a theory of consciousness unscientific?
Authors: Michał Klincewicz, Tony Cheng, Michael Schmitz, Miguel Ángel Sebastián, Joel S. Snyder, Derek H. Arnold, Mark G. Baxter, Tristan A. Bekinschtein, Yoshua Bengio, James W. Bisley, Jacob Browning, Dean Buonomano, David Carmel, Marisa Carrasco, Peter Carruthers, Olivia Carter, Dorita H. F. Chang, Ian Charest, Mouslim Cherkaoui, Axel Cleeremans, Michael A. Cohen, Philip R. Corlett, Kalina Christoff, Sam Cumming, Cody A. Cushing, Beatrice de Gelder, Felipe De Brigard, Daniel C. Dennett, Nadine Dijkstra, Adrien Doerig, Paul E. Dux, Stephen M. Fleming, Keith Frankish, Chris D. Frith, Sarah Garfinkel, Melvyn A. Goodale, Jacqueline Gottlieb, Jake R. Hanson, Ran R. Hassin, Michael H. Herzog, Cecilia Heyes, Po-Jang Hsieh, Shao-Min Hung, Robert Kentridge, Tomas Knapen, Nikos Konstantinou, Konrad Kording, Timo L. Kvamme, Sze Chai Kwok, Renzo C. Lanfranco, Hakwan Lau, Joseph LeDoux, Alan L. F. Lee, Camilo Libedinsky, Matthew D. Lieberman, Ying-Tung Lin, Ka-Yuet Liu, Maro G. Machizawa, Julio Martinez-Trujillo, Janet Metcalfe, Matthias Michel, Kenneth D. Miller, Partha P. Mitra, Dean Mobbs, Robert M. Mok, Jorge Morales, Myrto Mylopoulos, Brian Odegaard, Charles C.-F. Or, Adrian M. Owen, David Pereplyotchik, Franco Pestilli, Megan A. K. Peters, Ian Phillips, Rosanne L. Rademaker, Dobromir Rahnev, Geraint Rees, Dario L. Ringach, Adina Roskies, Daniela Schiller, Aaron Schurger, D. Samuel Schwarzkopf, Ryan B. Scott, Aaron R. Seitz, Joshua Shepherd, Juha Silvanto, Heleen A. Slagter, Barry C. Smith, Guillermo Solovey, David Soto, Hugo Spiers, Timo Stein, Vincent Taschereau-Dumouchel, Frank Tong, Peter U. Tse, Jonas Vibell, Sebastian Watzl, Taylor Webb, Josh Weisberg, Thalia Wheatley, Michał Wierzchoń, Martijn E. Wokke, Karen Yan
Journal: Nature Neuroscience (2025)
LILRB3 genetic variation is associated with kidney transplant failure in African American recipients
Authors: Zeguo Sun, Zhengzi Yi, Chengguo Wei, Wenlin Wang, Tianyuan Ren, Paolo Cravedi, Fasika Tedla, Stephen C. Ward, Evren Azeloglu, Daniel R. Schrider, Yun Li, Atlas Khan, Francesca Zanoni, Jia Fu, Sumaria Ali, Shun Liu, Deguang Liang, Tong Liu, Hong Li, Caixia Xi, Thi Ha Vy, Gohar Mosoyan, Quan Sun, Ashwani Kumar, Zhongyang Zhang, Samira Farouk, Kirk Campell, Jordi Ochando, Kyung Lee, Steve Coca, Jenny Xiang, Patti Connolly, Lorenzo Gallon, Philip J. O’Connell, Robert Colvin, Madhav C. Menon, Girish Nadkarni, John C. He, Monica Kraft, Xuejun Jiang, Xuewu Zhang, Krzysztof Kiryluk, Aravind Cherukuri, Fadi G. Lakkis, Weiguo Zhang, Shu-hsia Chen, Peter S. Heeger, Weijia Zhang
Journal: Nature Medicine (2025)
Pelabresib plus ruxolitinib for JAK inhibitor-naive myelofibrosis: a randomized phase 3 trial
Authors: Raajit K. Rampal, Sebastian Grosicki, Dominik Chraniuk, Elisabetta Abruzzese, Prithviraj Bose, Aaron T. Gerds, Alessandro M. Vannucchi, Francesca Palandri, Sung-Eun Lee, Vikas Gupta, Alessandro Lucchesi, Stephen T. Oh, Andrew T. Kuykendall, Andrea Patriarca, Alberto Álvarez-Larrán, Ruben Mesa, Jean-Jacques Kiladjian, Moshe Talpaz, Joseph M. Scandura, David Lavie, Morgan Harris, Sarah-Katharina Kays, Qing Li, Rainer Boxhammer, Barbara Brown, Anna-Maria Jegg, Claire N. Harrison, John Mascarenhas
Journal: Nature Medicine (2025)

Janus kinase (JAK) inhibitors provide limited depth and durability of response in myelofibrosis. We evaluated pelabresib—a bromodomain and extraterminal domain (BET) inhibitor—plus ruxolitinib (a JAK inhibitor) compared with placebo plus ruxolitinib as first-line therapy. In this phase 3 study (MANIFEST-2), JAK inhibitor-naive patients with myelofibrosis were randomized 1:1 to pelabresib 125 mg once daily (QD; 50–175 mg QD permitted) for 14 days followed by a 7-day break (21-day cycle), or to placebo in combination with ruxolitinib 10 or 15 mg twice daily (BID; 5 mg QD–25 mg BID permitted). Primary endpoint was reduction in spleen volume of ≥35% from baseline at week 24. Key secondary endpoints were absolute change in total symptom score (TSS) and TSS50 response (≥50% reduction in TSS from baseline at week 24). The primary endpoint was met in 65.9% of patients randomized to pelabresib–ruxolitinib (n = 214) versus 35.2% to placebo–ruxolitinib (n = 216) (difference, 30.4%; 95% confidence interval (CI), 21.6, 39.3; P < 0.001). Absolute change in TSS was −15.99 versus −14.05 (difference, −1.94; 95% CI, −3.92, 0.04; P = 0.0545) and TSS50 was achieved in 52.3% versus 46.3% (difference, 6.0%; 95 CI, −3.5, 15.5) with pelabresib–ruxolitinib versus placebo–ruxolitinib. Exploratory analyses of proinflammatory cytokine amounts and bone marrow morphology showed greater improvement with the combination. Thrombocytopenia and anemia were the most common treatment-emergent adverse events, occurring in 52.8% (13.2% grade ≥3) versus 37.4% (6.1% grade ≥3) and 44.8% (23.1% grade ≥3) versus 55.1% (36.5% grade ≥3), respectively. Pelabresib in combination with ruxolitinib is well tolerated, improves signs of underlying myelofibrosis pathobiology and provides substantial clinical benefit over standard-of-care JAK inhibitor monotherapy. ClinicalTrials.gov identifier: NCT04603495 . In a randomized phase 3 trial, the combination of the BET inhibitor pelabresib with the JAK inhibitor ruxolitinib resulted in a significantly higher spleen volume reduction from baseline versus placebo with ruxolitinib in patients with JAK inhibitor-naive myelofibrosis.
Consciousness or pseudo-consciousness? A clash of two paradigms
Authors: Giulio Tononi, Larissa Albantakis, Leonardo Barbosa, Melanie Boly, Chiara Cirelli, Renzo Comolatti, Francesco Ellia, Graham Findlay, Adenauer Girardi Casali, Matteo Grasso, Andrew M. Haun, Jeremiah Hendren, Erik Hoel, Christof Koch, Alexander Maier, William Marshall, Marcello Massimini, William GP Mayner, Masafumi Oizumi, Joanna Szczotka, Naotsugu Tsuchiya, Alireza Zaeemzadeh
Journal: Nature Neuroscience (2025)
Jordan eliminates leprosy disease and moves to post-elimination surveillance
Authors: Vivek Lal, Supriya Warusavithana, Daniel Argaw Dagne, Jamela Al-Raiby, Subbanna Jonnalagada, Chinara Aidyralieva, Ala’a Al-Shaikh, V. Ranganadha Rao Pemmaraju, Maya Ranavare, Rie Yotsu, Mourad Mokni, Feras Ibrahim Hawari
Journal: Nature Medicine (2025)
Allogeneic mesenchymal stem cell therapy with laromestrocel in mild Alzheimer’s disease: a randomized controlled phase 2a trial
Authors: Brian G. Rash, Kevin N. Ramdas, Nataliya Agafonova, Eric Naioti, Lisa McClain-Moss, Zarin Zainul, Brittany Varnado, Kevin Peterson, Michael Brown, Thiago Leal, Steven Kopcho, Raul Carballosa, Paayal Patel, Mark Brody, Brad Herskowitz, Ana Fuquay, Savannah Rodriguez, Alan F. Jacobson, Ramon Leon, Michael Pfeffer, Julie B. Schwartzbard, Jeffrey Botbyl, Anthony A. Oliva, Joshua M. Hare
Journal: Nature Medicine (2025)

Abstract Alzheimer’s disease (AD) is characterized by progressive cognitive decline, severe brain atrophy and neuroinflammation. We conducted a randomized, double-blind, placebo-controlled, parallel-group phase 2a clinical trial that tested the safety and efficacy of laromestrocel, a bone-marrow-derived, allogeneic mesenchymal stem-cell therapy, in slowing AD clinical progression, atrophy and neuroinflammation. Participants across ten centers in the United States were randomly assigned 1:1:1:1 to four infusion groups: group 1 (placebo; four monthly infusions, n = 12); group 2 (25 million cells, one infusion followed by three monthly infusions of placebo, n = 13); group 3 (25 million cells; four monthly doses, n = 13); and group 4 (100 million cells; four monthly doses, n = 11). The study met its primary end point of safety; the rate of treatment-emergent serious adverse events within 4 weeks of any infusion was similar in all four groups: group 1, 0% (95% CI 0–26.5%); group 2, 7.7% (95% CI 0.2–36%); group 3, 7.7% (95% CI 0.2–36%) and group 4, 9.1% (95% CI 0.2–41.3%). Additionally, there were no reported infusion-related reactions, hypersensitivities or amyloid-related imaging abnormalities. Laromestrocel improved clinical assessments at 39 weeks compared to placebo, as measured by a composite AD score (secondary end point was met: group 2 versus placebo change: 0.38; 95% CI −0.06–0.82), Montreal cognitive assessment and the Alzheimer’s Disease Cooperative Study Activities of Daily Living. At 39 weeks, Laromestrocel slowed the decline of whole brain volume compared to placebo ( n = 10) by 48.4% for all treatment groups combined (groups 2–4: P = 0.005; n = 32) and left hippocampal volume by 61.9% (groups 2–4, P = 0.021; n = 32), and reduced neuroinflammation as measured by diffusion tensor imaging. The change in bilateral hippocampal atrophy correlated with the change in mini-mental state exam scores ( R = 0.41, P = 0.0075) in all study patients ( N = 42). Collectively these results support safety of single and multiple doses of laromestrocel treatment for mild AD and provide indications of efficacy in combating decline of brain volume and potentially cognitive function. Larger-scale clinical trials of laromestrocel in AD are warranted. ClinicalTrials.gov registration: NCT05233774 .
Family-based genome-wide association study designs for increased power and robustness
Authors: Junming Guan, Tammy Tan, Seyed Moeen Nehzati, Michael Bennett, Patrick Turley, Daniel J. Benjamin, Alexander Strudwick Young
Journal: Nature Genetics (2025)

Abstract Family-based genome-wide association studies (FGWASs) use random, within-family genetic variation to remove confounding from estimates of direct genetic effects (DGEs). Here we introduce a ‘unified estimator’ that includes individuals without genotyped relatives, unifying standard and FGWAS while increasing power for DGE estimation. We also introduce a ‘robust estimator’ that is not biased in structured and/or admixed populations. In an analysis of 19 phenotypes in the UK Biobank, the unified estimator in the White British subsample and the robust estimator (applied without ancestry restrictions) increased the effective sample size for DGEs by 46.9% to 106.5% and 10.3% to 21.0%, respectively, compared to using genetic differences between siblings. Polygenic predictors derived from the unified estimator demonstrated superior out-of-sample prediction ability compared to other family-based methods. We implemented the methods in the software package snipar in an efficient linear mixed model that accounts for sample relatedness and sibling shared environment.
Guideline-compliant empirical antibiotic therapy for ventilator-associated pneumonia during the pandemic: a European multicenter retrospective study
Authors: Nicolas Dognon, Romain Malapelle, Maxime Leroy, Keyvan Razazi, Saad Nseir, Ignacio Martin-Loeches, Pedro Povoa, Antoni Torres, Demosthenes Makris, Fabien Lambiotte, Christophe Vinsonneau, Benoit Misset, Anahita Rouze, Luis Maia Morais, Deskata Konstantina, Flavia Galli, Antoine Gaillet, Pascale Labedade, Elsa Moncomble, Julien Labreuche, Darragh O’Reilly, Maité Perez, Anne Dewatine, Chaouki Bouras
Journal: Intensive Care Medicine (2025)
Engineering a stem cell-embedded bilayer hydrogel with biomimetic collagen mineralization for tendon-bone interface healing
Authors: Tingyun Lei, Tao Zhang, Tianshun Fang, Jie Han, Chunyi Gu, Youguo Liao, Yang Fei, Junchao Luo, Huanhuan Liu, Yan Wu, Weiliang Shen, Xiao Chen, Zi Yin, Junjuan Wang
Journal: Bioactive Materials (2025)
Microbiota transplant therapy in inflammatory bowel disease: advances and mechanistic insights
Authors: Daphne Moutsoglou, Pavithra Ramakrishnan, Byron P. Vaughn
Journal: Gut Microbes (2025)

Microbiota transplant therapy is an emerging therapy for inflammatory bowel disease, but factors influencing its efficacy and mechanism remain poorly understood. In this narrative review, we outline key elements affecting therapeutic outcomes, including donor factors (such as age and patient relationship), recipient factors, control selection, and elements impacting engraftment and its correlation with clinical response. We also examine potential mechanisms through inflammatory bowel disease trials, focusing on the interplay between the microbiota, host, and immune system. Finally, we briefly explore potential future directions for microbiota transplant therapy and promising emerging treatments.
A self-accelerating ‘copper bomb’ strategy activated innate and adaptive immune response against triple-negative breast cancer
Authors: Xinzhi Xu, Hang Zhou, Ruixia Hong, Jiaqi Gong, Yujie Wan, Qihuan Fu, Kaifeng Huang, Ying Li, Na Wang, Peng Zhao, Kaiyong Cai, Fang Li
Journal: Bioactive Materials (2025)
Association Between Cigarette Smoking and Subclinical Markers of Cardiovascular Harm
Authors: Zhiqi Yao, Erfan Tasdighi, Zeina A Dardari, Kunal K Jha, Ngozi Osuji, Tanuja Rajan, Ellen Boakye, Carlos J Rodriguez, Kunihiro Matsushita, Eleanor M Simonsick, Joao A C Lima, Rachel Widome, Debbie L Cohen, Lawrence J Appel, Amit Khera, Michael E Hall, Suzanne E Judd, Shelley A Cole, Ramachandran S Vasan, Emelia J Benjamin, Paulo A Lotufo, Isabela M Benseñor, Samar R El Khoudary, Emma Barinas-Mitchell, Imke Janssen, Bruce M Psaty, Charles B Eaton, Michael J LaMonte, Peggy M Cawthon, Eric S Orwoll, Marguerite R Irvin, Aruni Bhatnagar, Andrew P DeFilippis, Omar El-Shahaway, Michael J Blaha
Journal: Journal of the American College of Cardiology (2025)