tbuckley/cabot-search huggingface dataset:
Flortaucipir PET uncovers relationships between tau and amyloid-β in primary age–related tauopathy and Alzheimer’s disease
Authors: Keith A. Josephs, Nirubol Tosakulwong, Stephen D. Weigand, Jonathan Graff-Radford, Christopher G. Schwarz, Matthew L. Senjem, Mary M. Machulda, Kejal Kantarci, David S. Knopman, Aivi Nguyen, R. Ross Reichard, Dennis W. Dickson, Ronald C. Petersen, Val J. Lowe, Clifford R. Jack, Jennifer L. Whitwell
Journal: Science Translational Medicine (2024)

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Human iPSC–liver organoid transplantation reduces fibrosis through immunomodulation
Authors: Tomomi Tadokoro, Soichiro Murata, Mimoko Kato, Yasuharu Ueno, Tomonori Tsuchida, Ayumu Okumura, Yoshiki Kuse, Takahiro Konno, Yutaro Uchida, Yuriko Yamakawa, Marina Zushi, Megumi Yajima, Tatsuya Kobayashi, Shunsuke Hasegawa, Yumi Kawakatsu-Hatada, Yoshihito Hayashi, Shun Osakabe, Takuji Maeda, Kodai Kimura, Akihiro Mori, Maiko Tanaka, Yu Kamishibahara, Megumi Matsuo, Yun-Zhong Nie, Satoshi Okamoto, Takayoshi Oba, Naoki Tanimizu, Hideki Taniguchi
Journal: Science Translational Medicine (2024)

Donor organ shortages for transplantation remain a serious global concern, and alternative treatment is in high demand. Fetal cells and tissues have considerable therapeutic potential as, for example, organoid technology that uses human induced pluripotent stem cells (hiPSCs) to generate unlimited human fetal-like cells and tissues. We previously reported the in vivo vascularization of early fetal liver–like hiPSC-derived liver buds (LBs) and subsquent improved survival of recipient mice with subacute liver failure. Here, we show hiPSC–liver organoids (LOs) that recapitulate midgestational fetal liver promote de novo liver generation when grafted onto the surface of host livers in chemical fibrosis models, thereby recovering liver function. We found that fetal liver, a hematopoietic tissue, highly expressed macrophage-recruiting factors and antifibrotic M2 macrophage polarization factors compared with the adult liver, resulting in fibrosis reduction because of CD163 + M2-macrophage polarization. Next, we created midgestational fetal liver–like hiPSC-LOs by fusion of hiPSC-LBs to induce static cell-cell interactions and found that these contained complex structures such as hepatocytes, vasculature, and bile ducts after transplantation. This fusion allowed the generation of a large human tissue suitable for transplantation into immunodeficient rodent models of liver fibrosis. hiPSC-LOs showed superior liver function compared with hiPSC-LBs and improved survival and liver function upon transplantation. In addition, hiPSC-LO transplantation ameliorated chemically induced liver fibrosis, a symptom of liver cirrhosis that leads to organ dysfunction, through immunomodulatory effects, particularly on CD163 + phagocytic M2-macrophage polarization. Together, our results suggest hiPSC-LO transplantation as a promising therapeutic option for liver fibrosis.
Primary cilia mediate skeletogenic BMP and Hedgehog signaling in heterotopic ossification
Authors: Kai He, Heng Jiang, Weijun Li, Saman Toutounchi, Yan Huang, Jianfeng Wu, Xiaoyu Ma, Wolfgang Baehr, Robert J. Pignolo, Kun Ling, Xuhui Zhou, Haitao Wang, Jinghua Hu
Journal: Science Translational Medicine (2024)

Heterotopic ossification (HO), defined as the formation of extraskeletal bone in muscle and soft tissues, is a diverse pathological process caused by either genetic mutations or inciting trauma. Fibrodysplasia ossificans progressiva (FOP) is a genetic form of HO caused by mutations in the bone morphogenetic protein (BMP) type I receptor gene
Adjuvantation of a SARS-CoV-2 mRNA vaccine with controlled tissue-specific expression of an mRNA encoding IL-12p70
Authors: Byron Brook, Valerie Duval, Soumik Barman, Lauren Speciner, Cali Sweitzer, Asad Khanmohammed, Manisha Menon, Kimberly Foster, Pallab Ghosh, Kimia Abedi, Jacob Koster, Etsuro Nanishi, Lindsey R. Baden, Ofer Levy, Thomas VanCott, Romain Micol, David J. Dowling
Journal: Science Translational Medicine (2024)

Messenger RNA (mRNA) vaccines were pivotal in reducing severe acute respiratory syndrome 2 (SARS-CoV-2) infection burden, yet they have not demonstrated robust durability, especially in older adults. Here, we describe a molecular adjuvant comprising a lipid nanoparticle (LNP)–encapsulated mRNA encoding interleukin-12p70 (IL-12p70). The bioactive adjuvant was engineered with a multiorgan protection (MOP) sequence to restrict transcript expression to the intramuscular injection site. Admixing IL-12–MOP (CTX-1796) with the BNT162b2 SARS-CoV-2 vaccine increased spike protein–specific immune responses in mice. Specifically, the benefits of IL-12–MOP adjuvantation included amplified humoral and cellular immunity and increased immune durability for 1 year after vaccination in mice. An additional benefit included the restoration of immunity in aged mice to amounts comparable to those achieved in young adult animals, alongside amplification with a single immunization. Associated enhanced dendritic cell and germinal center responses were observed. Together, these data demonstrate that an LNP-encapsulated IL-12–MOP mRNA-encoded adjuvant can amplify immunogenicity independent of age, demonstrating translational potential to benefit vulnerable populations.
Targeting ferritinophagy impairs quiescent cancer stem cells in acute myeloid leukemia in vitro and in vivo models
Authors: Clement Larrue, Sarah Mouche, Paolo Angelino, Maxime Sajot, Rudy Birsen, Olivier Kosmider, Thomas Mckee, François Vergez, Christian Recher, Véronique Mansat-De Mas, Qiong Gu, Jun Xu, Petros Tsantoulis, Jean-Emmanuel Sarry, Jerome Tamburini
Journal: Science Translational Medicine (2024)

Acute myeloid leukemia (AML) remains a challenging hematological malignancy with poor prognosis and limited treatment options. Leukemic stem cells (LSCs) contribute to therapeutic failure, relapse, and adverse outcome. This study investigates the role of quiescence and related molecular mechanisms in AML pathogenesis and LSC functions to identify potential therapeutic targets. Transcriptomic analysis revealed that the LSC-enriched quiescent cell population has a distinct gene signature with prognostic relevance in patients with AML. Mechanistically, quiescent blasts exhibit increased autophagic activity, which contributes to their sustained viability. Proteomic profiling uncovered differential requirements for iron metabolism between quiescent and cycling cells, revealing a unique dependence of quiescent cells on ferritinophagy, a selective form of autophagy mediated by nuclear receptor coactivator 4 (NCOA4), which regulates iron bioavailability. We evaluated the therapeutic potential of inhibiting NCOA4-mediated ferritinophagy using genetic knockdown and chemical inhibition approaches. In vitro assays showed that suppression of NCOA4 was toxic to leukemic blasts, particularly the CD34 + CD38 − LSC-enriched population, without affecting normal CD34 + hematopoietic progenitors. In vivo studies using murine patient-derived xenograft (PDX) models of AML confirmed that NCOA4 inhibition reduced tumor burden and impaired LSC viability and self-renewal, indicating a specific vulnerability of these cells to ferritinophagy disruption. Our findings underscore the role of NCOA4-mediated ferritinophagy in maintaining LSC quiescence and function and suggest that targeting this pathway may be an effective therapeutic strategy for AML. This study highlights the potential of NCOA4 inhibition to improve AML outcomes and paves the way for future research and clinical development.
Early-Life Factors Associated With Adult-Onset Type 1 Diabetes: A Swedish Nationwide Cohort and Family-Based Study
Authors: Coralie Amadou, Yuxia Wei, Maria Feychting, Sofia Carlsson
Journal: Diabetes Care (2024)

Childhood-onset type 1 diabetes (T1D) is associated with perinatal factors, but data related to adult-onset T1D are scarce. This study aimed at investigating the association between early-life factors and adult-onset T1D in a Swedish nationwide cohort and family-based study.
A predictive model for therapy failure in chronic myeloid leukemia patients receiving tyrosine kinase inhibitor therapy
Authors: Xiaoshuai Zhang, Bingcheng Liu, Jian Huang, Yanli li Zhang, Na Xu, Robert Peter Gale, Weiming Li, Xiaoli Liu, Huanling Zhu, Ling Pan, Yunfan Yang, Hai Lin, Xin Du, Rong Liang, Chunyan Chen, Xiaodong Wang, Guohui Li, Zhougang Liu, Yanqing Zhang, Zhenfang Liu, Jianda Hu, Chunshui Liu, Fei Li, Wei Yang, Li Meng, Yanqiu Han, Li'e Lin, Zhenyu Zhao, Chuanqing Tu, Caifeng Zheng, Yanliang Bai, Zeping Zhou, Suning Chen, Huiying Qiu, Lijie Yang, Xiuli Sun, Hui Sun, Li Zhou, Zelin Liu, Danyu Wang, Jianxin Guo, Liping Pang, Qingshu Zeng, Xiaohui Suo, Weihua Zhang, Yuanjun Zheng, Xiaojun Huang, Qian Jiang
Journal: Blood (2024)

Abstract Although tyrosine kinase inhibitor (TKI) therapy has markedly improved the survival of people with chronic-phase chronic myeloid leukemia (CML), 20% to 30% of people still experienced therapy failure. Data from 1955 consecutive patients with chronic-phase CML diagnosed by the European LeukemiaNet recommendations from 1 center receiving initial imatinib or a second-generation (2G) TKI therapy were interrogated to develop a clinical prediction model for TKI-therapy failure. This model was subsequently validated in 3454 patients from 76 other centers. Using the predictive clinical covariates associated with TKI-therapy failure, we developed a model that stratified patients into low-, intermediate- and high-risk subgroups with significantly different cumulative incidences of therapy failure (P &amp;lt; .001). There was good discrimination and calibration in the external validation data set, and the performance was consistent with that of the training data set. Our model had the better prediction discrimination than the Sokal and European Treatment and Outcome Study long-term survival scores, with the greater time-dependent area under the receiver-operator characteristic curve values and a better ability to redefine the risk of therapy failure. Our model could help physicians estimate the likelihood of initial imatinib or 2G TKI–therapy failure in people with chronic-phase CML.
JAK2/mTOR Inhibition Fails to Prevent Acute GVHD Despite Reduced Th1/Th17 cells: Final Phase II Trial Results
Authors: Joseph A Pidala, Shernan G Holtan, Kelly Walton, Jongphil Kim, Biwei Cao, Hany Elmariah, Asmita Mishra, Nelli Bejanyan, Taiga Nishihori, Farhad Khimani, Lia E Perez, Rawan G Faramand, Marco L. Davila, Shannon McSain, Jordan Pleskow, Jeffrey Baron, Claudio Anasetti, Carlos M Moran Segura, Daniel J Weisdorf, Bruce R Blazar, Jeffrey S. Miller, Veronika Bachanova, Najla El Jurdi, Brian C Betts
Journal: Blood (2024)

Abstract Our phase 1 graft-versus-host disease (GVHD) prevention trial of JAK2 inhibitor, pacritinib (PAC; recommended phase 2 dose: 100 mg orally twice a day on day 0 to +70) plus sirolimus and tacrolimus (SIR/TAC) demonstrated the regimen was safe and free of pan-JAK myelosuppression after allogeneic hematopoietic cell transplantation (alloHCT). PAC inhibits interleukin 6 (IL-6) receptor activity and pathogenic T helper cell 1 (Th1)/Th17 differentiation in preclinical models and the phase 1 trial. Herein, we report on our completed phase 2 trial of PAC/SIR/TAC after 8/8 human leukocyte antigen matched alloHCT. This single-arm phase 2 trial (NCT02891603) was powered to determine if PAC/SIR/TAC suppressed percentage phosphorylated STAT3 (pSTAT3)+ CD4+ T cells at day +21 (primary end point: percentage pSTAT3+ CD4+ T cells ≤ 35%) and estimated grade II to IV acute GVHD by day +100. The impact of PAC/SIR/TAC on T-cell subsets, CD28 (pS6 and pH3ser10), and IL-2 receptor (pSTAT5) signal transduction was also evaluated. Eligible patients (n = 28) received alloHCT for hematologic malignancies or myeloproliferative neoplasms. Reduced or myeloablative intensity conditioning was permitted. PAC/SIR/TAC met the primary end point, reducing percentage pSTAT3+ CD4+ T cells to 9.62% at day +21. Th1/Th17 cells were decreased at day +21, increasing the ratio of regulatory T cells to Th1 and Th17 cells with PAC/SIR/TAC at recommended phase 2 dose PAC compared with dose level 1 PAC. The cumulative incidence of grade II to IV acute GVHD by day +100 with PAC/SIR/TAC was similar to historic SIR/TAC values (46% vs 43%). Although PAC/SIR/TAC suppressed pSTAT3 and Th1/Th17 cells, the regimen did not improve acute GVHD prevention.
Critical Role of Tripartite Fusion and LBD Truncation in Certain RARA- and all RARG-Related Atypical APL
Authors: Xiaosu Zhou, Xue Chen, Jiaqi Chen, Lijun Wen, Zhanglin Zhang, Ya-Zhen Qin, Panxiang Cao, Haizhou Xing, Yingchang Mi, Wei Wang, Guangsen Zhang, Ji Li, Huanling Wu, Zhifen Zhang, Jian Zhang, Zhan Su, Fang Wang, Yang Zhang, Xiaoli Ma, Jiancheng Fang, Ping Wu, Tong Wang, Gaowei Fan, Yang Zhao, David Jin, Xian Zhang, Xiujuan Ma, Qisheng Wu, Zhihua Zhang, Linya Wang, Futian Ma, Xia Xiao, Chengye Wu, Kai Sun, Ruijie Tang, Yun Zhang, Sanyun Wu, Ran Gao, Leping Zhang, Huyong Zheng, Yanli Zhao, Hong-Hu Zhu, Daopei Lu, Peihua Lu, Suning Chen, Hongxing Liu
Journal: Blood (2024)
Contribution of Clinical Trial Event Data by Data Source
Authors: Jennifer A. Rymer, Hillary Mulder, Lisa M. Wruck, Daniel Muñoz, Sunil Kripalani, Mark B. Effron, Kamal Gupta, Eileen Handberg, Sandeep Jain, Saket Girotra, Jeffrey Whittle, Rachel Hess, Catherine P. Benziger, Kirk U. Knowlton, Lesley H. Curtis, Matthew T. Roe, Bradley G. Hammill, Russell L. Rothman, Robert Harrington, Adrian Hernandez, W. Schuyler Jones
Journal: JAMA Cardiology (2024)

Importance Pragmatic randomized clinical trials (RCTs) often use multiple data sources to examine clinical events, but the relative contribution of data sources to clinical end-point rates is understudied. Objective To assess the contribution of data sources (electronic health records [EHRs], public/private insurance claims, and/or participant-reported data) to clinical end points among ADAPTABLE participants who had available data. Design, Setting, and Participants The ADAPTABLE study was an open-label, pragmatic RCT from April 2016 through June 2019 conducted in research networks within clinical practice. Participants had existing atherosclerotic cardiovascular disease and available data to analyze. The characteristics of patients by combinations of data source availability were compared to examine the contribution of each of the data sources to end-point ascertainment. Data for this prespecified analysis were examined from January 2022 to June 2023. Exposures Randomized exposure to 81 mg or 325 mg of aspirin daily. Main Outcomes and Measures Number of events for the primary end point (composite of death, hospitalization for myocardial infarction, and hospitalization for stroke) that were contributed by EHR or claims data and then number of events contributed by each additional data source. Results Of 15 006 participants randomized with at least 1 other source of data available beyond participant-reported data, there were 8756 (58.3%) with participant-reported and EHR data; 4291 (28.6%) with participant-reported, EHR, and claims data; 1412 (9.4%) with EHR-only data; 262 (1.7%) with participant-reported and claims data; 202 (1.3%) with EHR and claims data; and 83 (0.6%) with claims-only data. Participants with EHR-only data were younger (median age, 63.7 years; IQR, 55.8-71.4) compared with the other groups (range, 65.6-71.9 years). Among participants with both EHR and claims data, with or without participant-reported data (n = 4493), for each outcome, most events (92%-100%) were identified in the EHR or in claims data. For all clinical end points, participant-reported data contributed less than 10% of events not otherwise available from claims or EHR data. Conclusions and Relevance In this analysis of a pragmatic RCT, claims and EHR data provided the most clinical end-point data when compared with participant-reported events. These findings provide a framework for collecting end points in pragmatic clinical trials. Further work is needed to understand the data source combinations that most effectively provide clinical end-point data in RCTs.
Diagnostic Guidelines for Familial Hemophagocytic Lymphohistiocytosis Revisited
Authors: Jan-Inge Henter, Elena Sieni, Julia Eriksson, Elisabet Bergsten, Ida Hed Myrberg, Scott W. Canna, Maria Luisa Coniglio, Randy Q. Cron, Kate F. Kernan, Ashish R. Kumar, Kai Lehmberg, Francesca Minoia, Ahmed Naqvi, Angelo Ravelli, Yong-Min Tang, Matteo Bottai, Yenan T. Bryceson, AnnaCarin Horne, Michael B. Jordan
Journal: Blood (2024)

Abstract Current hemophagocytic lymphohistiocytosis 2004 (HLH-2004)–based diagnostic criteria for familial hemophagocytic lymphohistiocytosis (FHL) are based on expert opinion. Here, we performed a case-control study to test and possibly improve these criteria. We also developed 2 complementary expert opinion–based diagnostic strategies for FHL in patients with signs/symptoms suggestive of HLH, based on genetic and cellular cytotoxicity assays. The cases (N = 366) were children aged &amp;lt;16 years with verified familial and/or genetic FHL (n = 341) or Griscelli syndrome type 2 (n = 25); 276 from the HLH-94/HLH-2004 databases and 90 from the Italian HLH Registry. All fulfilled the HLH-94/HLH-2004 patient inclusion criteria. Controls were 374 children with systemic-onset juvenile idiopathic arthritis (sJIA) and 329 + 361 children in 2 cohorts with febrile infections that could be confused with HLH and sepsis, respectively. To provide complete data sets, multiple imputations were performed. The optimal model, based on 17 variables studied, revealed almost similar diagnostic thresholds as the existing criteria, with accuracy 99.1% (sensitivity 97.1%; specificity 99.5%); the original HLH-2004 criteria had accuracy 97.4% (sensitivity 99.0%; specificity 97.1%). Because cellular cytotoxicity assays here constitute a separate diagnostic strategy, HLH-2004 criteria without natural killer (NK)–cell function was also studied, which showed accuracy 99.0% (sensitivity, 96.2%; specificity, 99.5%). Thus, we conclude that the HLH-2004 criteria (without NK-cell function) have significant validity in their current form when tested against severe infections or sJIA. It is important to exclude underlying malignancies and atypical infections. In addition, complementary cellular and genetic diagnostic guidelines can facilitate necessary confirmation of clinical diagnosis.
Dapagliflozin and Right Ventricular–Pulmonary Vascular Interaction in Heart Failure With Preserved Ejection Fraction
Authors: Yogesh N. V. Reddy, Rickey E. Carter, Hidemi Sorimachi, Massar Omar, Dejana Popovic, Alessio Alogna, Michael D. Jensen, Barry A. Borlaug
Journal: JAMA Cardiology (2024)

Increases in pulmonary capillary wedge pressure (PCWP) during exercise reduce pulmonary artery (PA) compliance, increase pulsatile right ventricular (RV) afterload, and impair RV-PA coupling in patients with heart failure with preserved ejection fraction (HFpEF). The effects of the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin on pulmonary vascular properties and RV-PA coupling are unknown.
Clinical phenotypes and short-term outcomes based on prehospital point-of-care testing and on-scene vital signs
Authors: Raúl López-Izquierdo, Carlos del Pozo Vegas, Ancor Sanz-García, Agustín Mayo Íscar, Miguel A. Castro Villamor, Eduardo Silva Alvarado, Santos Gracia Villar, Luis Alonso Dzul López, Silvia Aparicio Obregón, Rubén Calderon Iglesias, Joan B. Soriano, Francisco Martín-Rodríguez
Journal: npj Digital Medicine (2024)

Abstract Emergency medical services (EMSs) face critical situations that require patient risk classification based on analytical and vital signs. We aimed to establish clustering-derived phenotypes based on prehospital analytical and vital signs that allow risk stratification. This was a prospective, multicenter, EMS-delivered, ambulance-based cohort study considering six advanced life support units, 38 basic life support units, and four tertiary hospitals in Spain. Adults with unselected acute diseases managed by the EMS and evacuated with discharge priority to emergency departments were considered between January 1, 2020, and June 30, 2023. Prehospital point-of-care testing and on-scene vital signs were used for the unsupervised machine learning method (clustering) to determine the phenotypes. Then phenotypes were compared with the primary outcome (cumulative mortality (all-cause) at 2, 7, and 30 days). A total of 7909 patients were included. The median (IQR) age was 64 (51–80) years, 41% were women, and 26% were living in rural areas. Three clusters were identified: alpha 16.2% (1281 patients), beta 28.8% (2279), and gamma 55% (4349). The mortality rates for alpha , beta and gamma at 2 days were 18.6%, 4.1%, and 0.8%, respectively; at 7 days, were 24.7%, 6.2%, and 1.7%; and at 30 days, were 33%, 10.2%, and 3.2%, respectively. Based on standard vital signs and blood test biomarkers in the prehospital scenario, three clusters were identified: alpha (high-risk), beta and gamma (medium- and low-risk, respectively). This permits the EMS system to quickly identify patients who are potentially compromised and to proactively implement the necessary interventions.
KDM6A Regulates Immune Response Genes in Multiple Myeloma
Authors: Daphné Dupéré-Richer, Alberto Riva, Benjamin G. Barwick, Sayantan Maji, Heidi Casellas Román, Jianping Li, Umasankar De, Amin Sobh, Gabrielle Quickstad, Crissandra Piper, Marta Kulis, Teresa Ezponda, José Ignacio Martín-Subero, Giovanni Tonon, Weizhou Zhang, Constantine S. Mitsiades, Lawrence H. Boise, Richard L. Bennett, Jonathan D. Licht
Journal: Blood (2024)
Ruxolitinib for pediatric patients with treatment-naïve and steroid-refractory acute graft-versus-host disease (REACH4)
Authors: Franco Locatelli, Hyoung Jin Kang, Bénédicte Bruno, Virginie Gandemer, Fanny Rialland, Maura Faraci, Yoshiyuki Takahashi, Katsuyoshi Koh, Henrique Bittencourt, Grace Cleary, Christine Rosko, Xuechan Li, Annie St Pierre, Anirudh Prahallad, Cristina Diaz-de-Heredia
Journal: Blood (2024)
Interleukin-1 blockade in patients with Wiskott-Aldrich Syndrome: a retrospective multinational case series
Authors: Samuele Naviglio, Maria Pia Cicalese, Elizabeth Rivers, Francesca Ferrua, Carmem M.S. Bonfim, Sabina Cenciarelli, Kai-Ning Cheong, Maura Faraci, Stefano Giardino, Sujal Ghosh, Pamela P. Lee, Paula Teixeira Lyra, Roland Meisel, Valentina Sofia, Antimo Tessitore, Alberto Tommasini, Erica Valencic, Tanja C. Vallée, Stefano Volpi, Austen J Worth, Marco Rabusin, Michael H Albert, Adrian J Thrasher, Alessandro Aiuti
Journal: Blood (2024)
Symptoms of Posttraumatic Stress Disorder Among Japanese Peacekeepers Deployed in South Sudan
Authors: Masato Kitano, Erik J. Giltay, Taku Saito, Florentine H. S. van der Does, Toshinori Chiba, Eric Vermetten, Naoki Edo, Fumiko Waki, Minori Koga, Hiroyuki Toda, Nic J. van der Wee, Masanori Nagamine
Journal: JAMA Network Open (2024)

Peacekeepers in United Nations missions experience potentially traumatic events, resulting in increased risk for posttraumatic stress disorder (PTSD). Understanding the course and risk factors of PTSD symptom severity is crucial to ensure personnel safety.
Medication for Opioid Use Disorder After Serious Injection-Related Infections in Massachusetts
Authors: Simeon D. Kimmel, Alexander Y. Walley, Laura F. White, Shapei Yan, Christine Grella, Adam Majeski, Michael D. Stein, Amy Bettano, Dana Bernson, Mari-Lynn Drainoni, Jeffrey H. Samet, Marc R. Larochelle
Journal: JAMA Network Open (2024)

Serious injection-related infections (SIRIs) cause significant morbidity and mortality. Medication for opioid use disorder (MOUD) improves outcomes but is underused. Understanding MOUD treatment after SIRIs could inform interventions to close this gap.