tbuckley/cabot-search huggingface dataset:
Trapα deficiency impairs the early events of insulin biosynthesis and glucose homeostasis
Authors: Xin Li, Jingxin Hu, Yumeng Huang, Hai Zhang, Ning Xu, Yang Liu, Xuan Liu, Yuanyuan Ye, Xinxin Zhang, Xiaoxi Xu, Yuxin Fan, Ziyue Zhang, Weiping J Zhang, Shusen Wang, Wenli Feng, Peter Arvan, Ming Liu
Journal: Journal of Clinical Investigation (2025)

Defects in the early events of insulin biosynthesis, including inefficient preproinsulin (PPI) translocation across the membrane of the endoplasmic reticulum (ER) and proinsulin (PI) misfolding in the ER, can cause diabetes. Cellular machineries involved in these events remain poorly defined. Gene encoding TRanslocon-Associated Protein alpha (TRAPα) shows linkage to glycemic control in humans, although their pathophysiological role remains unknown. Here we found that β-cell specific TRAPα knockout (TRAPα-βKO) mice fed with chow diet or high fat diet (HFD) exhibit decreased circulating insulin, with age- and diet-related glucose intolerance. Multiple independent approaches revealed that TRAPα-βKO not only causes inefficient PPI translocation, but also leads to PI misfolding and ER stress, selectively limiting PI ER export and β-cell compensatory potential. Importantly, decreased TRAPα expression was evident in islets of wild-type mice fed with high fat diet and in patients with type 2 diabetes (T2D). Furthermore, TRAPα expression was positively correlated with insulin content in human islet β cells, and decreased TRAPα was associated with PI maturation defects in T2D islets. Together, these data demonstrate that TRAPα deficiency in pancreatic β-cells impairs PPI translocation, PI folding, insulin production, and glucose homeostasis, contributing to its genetic linkage to T2D.
Integrin-mediated mTOR signaling drives TGF-β overactivity and myxomatous mitral valve degeneration in hypomorphic fibrillin-1 mice
Authors: Fu Gao, Qixin Chen, Makoto Mori, Sufang Li, Giovanni Ferrari, Markus Krane, Rong Fan, George Tellides, Yang Liu, Arnar Geirsson
Journal: Journal of Clinical Investigation (2025)

Mitral valve prolapse is often benign but progression to mitral regurgitation may require invasive intervention and there is no specific medical therapy. An association of mitral valve prolapse with Marfan syndrome resulting from pathogenic FBN1 variants supports the use of hypomorphic fibrillin-1 mgR mice to investigate mechanisms and therapy for mitral valve disease. mgR mice developed severe myxomatous mitral valve degeneration with mitral regurgitation by 12 weeks of age. Persistent activation of TGF-β and mTOR signaling along with macrophage recruitment preceded histological changes at 4 weeks of age. Short-term mTOR inhibition with rapamycin from 4 to 5 weeks of age prevented TGF-β overactivity and leukocytic infiltrates, while long-term inhibition of mTOR or TGF-β signaling from 4 to 12 weeks of age rescued mitral valve leaflet degeneration. Transcriptomic analysis identified integrins as key receptors in signaling interactions and serologic neutralization of integrin signaling or a chimeric integrin receptor altering signaling prevented mTOR activation. We confirmed increased mTOR signaling and a conserved transcriptome signature in human specimens of sporadic mitral valve prolapse. Thus, mTOR activation from abnormal integrin-dependent cell-matrix interactions drives TGF-β overactivity and myxomatous mitral valve degeneration, and mTOR inhibition may prevent disease progression of mitral valve prolapse.
Phospho-RPA2 predicts response to platinum and PARP inhibitors in homologous recombination-proficient ovarian cancer
Authors: Angela Schab, Amanda Compadre, Rebecca Drexler, Megan Loeb, Kevin Rodriguez, Joshua Brill, Shariska Harrington, Carmen Sandoval, Brooke Sanders, Lindsay Kuroki, Carolyn McCourt, Andrea R Hagemann, Premal Thaker, David Mutch, Matthew Powell, Violeta Serra, Ian S Hagemann, Ann E Walts, Beth Y Karlan, Sandra Orsulic, Katherine Fuh, Lulu Sun, Priyanka Verma, Elena Lomonosova, Peinan Zhao, Dineo Khabele, Mary M Mullen
Journal: Journal of Clinical Investigation (2025)

Treatment of tubo-ovarian high-grade serous carcinoma (HGSC) includes cytoreductive surgery, platinum-based chemotherapy, and often poly (ADP-ribose) polymerase (PARP) inhibitors. While homologous recombination (HR)-deficiency is a well-established predictor of therapy sensitivity, over 50% of HR-proficient HGSC also exhibit sensitivity. Currently, there are no biomarkers to identify which HR-proficient HGSCs will be sensitive to standard-of-care therapy. Replication stress may serve as a key determinant of response. We evaluated phospho-RPA2-T21 (pRPA2) foci via immunofluorescence as a biomarker of replication stress in formalin-fixed, paraffin-embedded HGSC samples collected at diagnosis from patients treated with platinum chemotherapy (discovery cohort: n=31, validation cohort: n=244) or PARP inhibitors (n=63). Recurrent HGSCs (n=38) were also analyzed. pRPA2 score was calculated using automated imaging analysis. Samples were defined as pRPA2-High if >16% of cells had ≥2 pRPA2 foci on automated analysis. In the discovery cohort, HR-proficient, pRPA2-High HGSCs demonstrated significantly higher rates of a chemotherapy response score of 3 to platinum chemotherapy than HR-proficient, pRPA2-Low HGSCs. In the validation cohort, patients with HR-proficient, pRPA2-High HGSCs had significantly longer survival after platinum treatment than those with HR-proficient, pRPA2-Low HGSCs. Additionally, the pRPA2 assay effectively predicted survival outcomes in patients treated with PARP inhibitors and in recurrent HGSC samples. Our study underscores the importance of considering replication stress marker, such as pRPA2, alongside HR status in therapeutic planning. This approach has the potential to increase the number of patients receiving effective therapy while reducing unnecessary toxicity.
Nephrotoxicity Surveillance for Childhood and Young Adult Survivors of Cancer: Recommendations From the International Late Effects of Childhood Cancer Guideline Harmonization Group
Authors: Esmee C.M. Kooijmans, Renée L. Mulder, Stephen D. Marks, Vesna Pavasovic, Shveta S. Motwani, Thomas Walwyn, Nicholas G. Larkins, Jarmila Kruseova, Louis S. Constine, W. Hamish Wallace, Daniel M. Green, Arend Bökenkamp, Helena J.H. van der Pal, Marry M. van den Heuvel-Eibrink, Lars Hjorth, Liv Andrés-Jensen, Edit Bardi, Elvira C. van Dalen, Charlotte Demoor-Goldschmidt, Kerri Becktell, Marika Grönroos, Kathleen Kieran, Denitza Mironova, Monica Terenziani, Margreet A. Veening, Jakub Zieg, Songul Onder, Ali Mirza Onder, Jonathan C. Routh, Joel Thompson, Melissa M. Hudson, Leontien C.M. Kremer, Roderick Skinner, Matthew J. Ehrhardt
Journal: Journal of Clinical Oncology (2025)

PURPOSE Childhood, adolescent, and young adult (CAYA) survivors of cancer are at risk of nephrotoxicity. Surveillance guidelines are important for timely diagnosis and treatment of these survivors, which could slow the progression to higher stages of kidney dysfunction. METHODS The International Late Effects of Childhood Cancer Guideline Harmonization Group established a multidisciplinary panel of 34 experts from 11 countries. The panel performed systematic literature reviews for articles published between 1990 and June 2023, graded the evidence using Grading of Recommendations Assessment, Development, and Evaluation methodology, and formulated recommendations based on evidence, clinical judgment, and consideration of benefits and harms of surveillance. Recommendations were critically appraised by two independent external experts and patient representatives. RESULTS Glomerular dysfunction surveillance is recommended every 2-5 years for survivors treated with ifosfamide, cisplatin, abdominal radiotherapy, total body irradiation, or nephrectomy and is reasonable after carboplatin treatment. We recommend screening for glomerular dysfunction using an estimated glomerular filtration rate (eGFR) equation that includes serum creatinine, preferably combined with serum cystatin C if available. Tubular dysfunction surveillance is recommended once at entry into long-term follow-up and with follow-up as clinically indicated for survivors treated with ifosfamide and is reasonable after cisplatin treatment. CONCLUSION These recommendations inform routine, uniform long-term follow-up care for CAYA survivors of cancer at risk of nephrotoxicity.
Analysis of drug consumption and expenditure of WHO essential medicines for cancer in 40 countries and regions between 2012 and 2022: a multinational drug use study
Authors: Yuanshi Jiao, Lin Bai, Jiaqi Wang, Vincent Ka Chun Yan, Esther W Chan, Rong Na, David Makram Bishai, Xiaodong Guan, Xue Li
Journal: The Lancet Oncology (2025)
A call to action: the second Lancet Commission on adolescent health and wellbeing
Authors: Sarah Baird, Shakira Choonara, Peter S Azzopardi, Prerna Banati, Judith Bessant, Olivia Biermann, Anthony Capon, Mariam Claeson, Pamela Y Collins, Nicole De Wet-Billings, Surabhi Dogra, Yanhui Dong, Kate L Francis, Luwam T Gebrekristos, Allison K Groves, Simon I Hay, David Imbago-Jácome, Aaron P Jenkins, Caroline W Kabiru, Elissa C Kennedy, Luo Li, Chunling Lu, Jun Ma, Terry McGovern, Augustina Mensa-Kwao, Sanyu A Mojola, Jason M Nagata, Adesola O Olumide, Olayinka Omigbodun, Molly O'Sullivan, Audrey Prost, Jennifer H Requejo, Yusra R Shawar, Jeremy Shiffman, Avi Silverman, Yi Song, Sharlene Swartz, Rita Tamambang, Henrik Urdal, Joseph L Ward, George C Patton, Susan M Sawyer, Alex Ezeh, Russell M Viner
Journal: The Lancet (2025)
A new characterisation of acute traumatic brain injury: the NIH-NINDS TBI Classification and Nomenclature Initiative
Authors: Geoffrey T Manley, Kristen Dams-O'Connor, Michael L Alosco, Hibah O Awwad, Jeffery J Bazarian, Peter Bragge, John D Corrigan, Adele Doperalski, Adam R Ferguson, Christine L Mac Donald, David K Menon, Molly M McNett, Joukje van der Naalt, Lindsay D Nelson, Dana Pisică, Noah D Silverberg, Nsini Umoh, Lindsay Wilson, Esther L Yuh, Henrik Zetterberg, Andrew I R Maas, Michael A McCrea
Journal: The Lancet Neurology (2025)
Sepsis in patients who are immunocompromised: diagnostic challenges and future therapies
Authors: Stefanie Deinhardt-Emmer, Benjamin G Chousterman, Joerg C Schefold, Stefanie B Flohé, Tomasz Skirecki, Matthijs Kox, Martin S Winkler, Andrea Cossarizza, W Joost Wiersinga, Tom van der Poll, Markus A Weigand, Sara Cajander, Evangelos J Giamarellos-Bourboulis, Gunnar Lachmann, Massimo Girardis, Brendon P Scicluna, Ricard Ferrer, Didier Payen, Sebastian Weis, Antoni Torres, Jesús F Bermejo-Martín, Marcin F Osuchowski, Ignacio Rubio, Hjalmar R Bouma
Journal: The Lancet Respiratory Medicine (2025)
Moving the dial on diagnostics: an update from the Lancet Commission on diagnostics
Authors: Susan Horton, Michael L Wilson, Annie N Y Cheung, Kristen DeStigter, Mikashmi Kohli, Shahin Sayed, Lee F Schroeder, Richard Sullivan, Bien-Soo Tan, Millicent Alooh, Bernice Dahn, Lluis Donoso-Bach, Patricia J Garcia, Sarwat Hussain, Kekeletso Kao, Lai-Meng Looi, Madhukar Pai, Mario Plebani, Yenew Kebede Tebeje, Grace Umutesi, Kamini Walia, Kenneth A Fleming
Journal: The Lancet (2025)
Safety and pharmacokinetics of N6LS, a broadly neutralising monoclonal antibody for HIV: a phase 1, open-label, dose-escalation study in healthy adults
Authors: Richard L Wu, Katherine V Houser, Martin R Gaudinski, Alicia T Widge, Seemal F Awan, Cristina A Carter, LaSonji A Holman, Jamie Saunders, Cynthia S Hendel, Aba Eshun, William R Whalen, Xiaolin Wang, Anita Arthur, Jennifer E Cunningham, Allison Beck, Joseph P Casazza, Galina V Yamshchikov, Ro Shauna Rothwell, Larisa Strom, Tejaswi Dittakavi, Myra Happe, Somia P Hickman, Michelle Conan-Cibotti, Kevin Carlton, Lily Zhang, Yunda Huang, Edmund V Capparelli, Mike Castro, Bob C Lin, Sarah O'Connell, Britta S Flach, Robert T Bailer, Sandeep R Narpala, Leonid Serebryannyy, Adrian B McDermott, Frank J Arnold, Jason G Gall, Sandra Vazquez, Nina M Berkowitz, Ingelise J Gordon, Grace L Chen, Peter D Kwong, Jinghe Huang, Theodore C Pierson, Mark Connors, John R Mascola, Tongqing Zhou, Nicole A Doria-Rose, Richard A Koup, Lesia K Dropulic, Julie E. Ledgerwood, Barney S. Graham, Emily E. Coates, Krisha McKee, Mark Louder, Amarendra Pegu, Niharika Shah, Floreliz Mendoza, Pamela Costner, Laura Novik, Kathy Zephir, Brenda Larkin, Sarah Plummer, Abidemi Ola, Preeti Apte, Cora Trelles Cartagena, Renunda Dyer, Pernell Williams, Shinyi Telscher, Colin Tran, Olga Vasilenko, Karen Parker, Priya Kamath, Jennifer Phipps, Olympia Hotobah-During, Jackie Stephens, Justine Jones, Jumoke Gbadebo, Catina Evans, Sandra Sitar, Christian Buettner, Sana Waheed, Maria Burgos Florez, Eugeania Burch, Lam Le, Olga Trofymenko, Patricia Morgan, Mark O'Callahan, Ellie Seo, Lauren Brant, Iris Pittman, Katherine Brooks, Martha Nason, Ana Villa-Ortega, Thuy Nguyen, Alison Taylor, Lucio Gama, Florence Kaltovich, Jason Sands, Christopher Case, Judy Stein
Journal: The Lancet HIV (2025)
Extended CT angiography versus standard CT angiography for the detection of cardioaortic thrombus in patients with ischaemic stroke and transient ischaemic attack (DAYLIGHT): a prospective, randomised, open-label, blinded end-point trial
Authors: Luciano A Sposato, Diana Ayan, Mobeen Ahmed, Sebastian Fridman, Jennifer L Mandzia, Maged Elrayes, Facundo Lodol, Alexander V Khaw, Lauren M Mai, Chrysi Bogiatzi, Courtney Casserly, J Alexander Fraser, Richard Chan, Anita Florendo Cumbermack, Nevena Markovic, Yeyao Yu, Derek Debicki, Lorraine Fleming, Beth Beauchamp, Lindsay Lambourn, Michael Mayich, Lindsay Milroy, Manas Sharma, Sachin Pandey, Rodrigo Bagur
Journal: The Lancet Neurology (2025)
Leisure-time physical activity after diagnosis and survival by cancer type: a pooled analysis
Authors: Erika Rees-Punia, Lauren R Teras, Christina C Newton, Steven C Moore, I-Min Lee, Lauren Bates-Fraser, Den E Bloodworth, A Heather Eliassen, Lorelei Mucci, Brigid M Lynch, Meir Stampfer, Mingyang Song, Kristen D Brantley, Konrad H Stopsack, Charles E Matthews, Alpa V Patel
Journal: JNCI Journal of the National Cancer Institute (2025)

Abstract Purpose Evidence for potential mortality benefits of leisure-time moderate-to-vigorous intensity physical activity (MVPA) for survivors of cancer types beyond breast and colorectal is limited. The aim of this study was to evaluate relationships between postdiagnosis MVPA and all-cause mortality in participants with a history of eleven cancer types. Methods Data were pooled from six United States-based cohort studies. Cohort-specific hazard ratios and 95% confidence intervals (HR, CI) for associations of MVPA assessed ≥1-year after a cancer diagnosis and all-cause mortality were calculated using multivariable Cox proportional hazards models and then pooled using random effects meta-analysis. Models were adjusted for age, sex, race/ethnicity, smoking status, alcohol use, cancer treatment and stage. The sample included 90,844 cancer survivors (mean [standard deviation] age at diagnosis = 67 [10] years, 55% women), among whom 45,477 died during 10.9 [7.0] years of follow-up. Results Compared to no MVPA, engaging in recommended amounts of MVPA (7.5-&amp;lt;15 MET-hr./wk.) was related to better overall survival in participants with a history of one of ten cancer types: oral (HR = 0.44, 0.27-0.73), endometrial (0.50, 0.34-0.76), lung (0.51, 0.38-0.68), rectal (0.51, 0.36-0.71), respiratory (0.51, 0.29-0.72), bladder (0.53, 0.40-0.72), kidney (0.53, 0.37-0.77), prostate (0.60, 0.49-0.74), colon (0.61, 0.50-0.76), and breast (0.67, 0.55-0.81). Eight of the ten observed inverse associations remained similar when excluding participants who died within two years of follow-up. Conclusion Engaging in leisure-time MVPA after a cancer diagnosis appears to improve survival for people with a history of several cancer types, including bladder, breast, colon, endometrial, kidney, lung, oral, prostate, rectal, and respiratory cancer.
Early Postoperative Minimal Residual Disease Detection with MAESTRO Is Associated with Recurrence and Worse Survival in Patients with Head and Neck Cancer
Authors: Edward S. Sim, Justin Rhoades, Kan Xiong, Laurel Walsh, Andjela Crnjac, Timothy Blewett, Yana Al-Inaya, Julia Mendel, Daniel A. Ruiz-Torres, Vasileios Efthymiou, Gjystina Lumaj, William J. Benjamin, G. Mike Makrigiorgos, Shervin Tabrizi, Viktor A. Adalsteinsson, Daniel L. Faden
Journal: Clinical Cancer Research (2025)

Abstract Purpose: Although ctDNA is a promising biomarker for minimal residual disease (MRD) detection in head and neck squamous cell carcinoma (HNSCC), more sensitive assays are needed for accurate MRD detection at clinically relevant time points. Ultrasensitive MRD detection early after surgery could guide adjuvant therapy decisions, but early ctDNA dynamics are poorly understood. Experimental Design: We applied minor allele–enriched sequencing through recognition oligonucleotides (MAESTRO), a whole-genome, tumor-informed, mutation enrichment sequencing assay, in a pooled testing format called MAESTRO-Pool, to plasma samples from patients with HNSCC collected shortly after surgery and during surveillance. We evaluated whether early MRD detection could predict outcomes. Results: Among 24 patients with predominantly human papillomavirus–independent (95.8%) HNSCC, rapid ctDNA clearance occurred by the first postoperative sample (1–3 days postoperatively) in nine patients without an event (recurrence or death). Thirteen of fifteen patients with an event were MRD-positive (positive predictive value = 92.9%; negative predictive value = 80%) with a median tumor fraction (TFx) of 54 parts per million (ppm; range 6–1,177 ppm). In the first and last samples of the early postoperative window, 8/13 and 10/13 patients, respectively, had TFx below 100 ppm, the detection limit of leading commercial assays. Early MRD detection correlated with worse overall survival (HR, 8.3; 95% confidence interval, 1.1–66.1; P = 0.02) and event-free survival (HR, 27.4; 95% confidence interval, 3.5–214.5; P &amp;lt; 0.0001) independent of high-risk pathology. Conclusions: Early postoperative MRD detection by MAESTRO was associated with recurrence and worse survival. Given the ultralow TFxs observed, ultrasensitive assays will be essential for reliable MRD detection during early postoperative time points to enable personalized adjuvant therapy decision-making in HNSCC. See related article by Bryan et al., p. XX .
Suppressing MASH fibrotic progression by blocking succinate-GPR91 signaling in hepatic stellate cells
Authors: Li Xie, Hui Chen, Li Zhang, Yong-Yu Yang, Yuan Zhou, Yue Ma, Chang Liu, Yu-Li Wang, Qin Zhu, Ya-Jun Yan, Jia Ding, Ning-Ping Zhang, Qiang Deng, Xiu-Ping Liu, Wei Jiang, Jian Wu
Journal: Hepatology (2025)

Background: The succinate receptor GPR91 is highly expressed in hepatic stellate cells (HSCs), with its expression further elevated during metabolic-dysfunction-associated steatohepatitis (MASH)-induced fibrotic progression. However, convincing in vivo data on whether blocking GPR91 signaling leads to fibrotic regression in MASH is lacking. Methods: MASH models were induced by choline-deficient amino acid-defined diet feeding along with lipopolysaccharide injection (CDAA-LPS) plus intraperitoneal injection of succinate or by high-fat and high-calorie diet plus high fructose and glucose in drinking water (HFCD-HF/G) in wild-type (WT) mice and HSC-specific GPR91 knockout (HSC-GPR91-KO) mice. Results: Administration of succinate significantly exacerbated fibrosis in CDAA-fed WT mice, as evidenced by increased collagen deposition and hydroxyproline levels along with an increased GPR91 expression in activated HSCs. Both WT and HSC-GPR91-KO mice exhibited substantial elevation in hepatic succinate levels upon HFCD-HF/G diet feeding. However, in comparison to HFCD+HF/G-fed WT mice, hepatic fibrosis was markedly ameliorated in HSC-GPR91-KO mice, as evidenced by diminished hepatic hydroxyproline content with downregulated fibrogenic markers. Succinate stimulation led to an increase in α-SMA, GPR91, phosphorylated ERK1/2, c-jun and Smad3 protein levels and enhanced the molecular interaction between c-jun and Smad3, inhibited forskolin-induced cAMP production in human HSCs, and increased p-NF-κB transcriptional activity, thereby suppressing HSC apoptosis. Conclusions: HSC-specific GPR91 receptor deficiency effectively halted hepatic fibrosis, probably through two distinct signaling pathways: suppressing the succinate-GPR91-Gβγ-ERK/c-jun-smad3 axis that positively regulates HSC activation; and abrogating the GPR91-Gαi-cAMP-NF-κB pathway that hinders their apoptosis. These findings confer GPR91 as a promising target for molecular interventions in blocking MASH-fibrotic progression.
TATA-box binding protein associated factor 2 (TAF2) in hepatocyte survival and tumorigenesis
Authors: Saranya Chidambaranathan Reghupaty, Suchismita Raha, Rachel Mendoza, Debashri Manna, Ali Gawi Ermi, Eva Davis, Younus Aqeel, Mark A. Subler, Jennifer Koblinski, Michael Idowu, Nitai Mukhopadhyay, Zhao Lai, Paul B. Fisher, Jolene J. Windle, Mikhail G. Dozmorov, Devanand Sarkar
Journal: Hepatology (2025)

Chromosome 8q amplification is a frequent event in cancers including hepatocellular carcinoma (HCC). TATA-box binding protein Associated Factor 2 (TAF2), a component of Transcription Factor IID (TFIID) residing in 8q24.12, is amplified in HCC. As yet, a potential oncogenic function of TAF2 in HCC has not been documented. We identified TAF2 mRNA and protein overexpression in human HCC cells and tissue samples, compared to their normal counterparts. A significant negative correlation between TAF2 levels and overall survival of HCC patients was observed. The role of TAF2 in HCC regulation was examined using a hepatocyte-specific conditional knockout mouse (Taf2 ΔHEP ), TAF2 knockdown and overexpressing human HCC cells, and TAF2 overexpression in mouse liver by hydrodynamic approach. As a core component of basal transcription machinery, TAF2 is required for hepatocyte survival. As such, in Taf2 ΔHEP mice there were hepatocyte death and compensatory proliferation, contributing to an inflammatory/fibrotic milieu favoring HCC. Accordingly, N-nitrosodiethylamine (DEN)/high fat high sugar diet-induced HCC was robustly augmented in Taf2 ΔHEP mice compared to their wild-type littermates. TAF2 overexpression in mouse liver did not lead to tumor development, but significantly augmented HCC that was induced by overexpression of the driver oncogene MYC. TAF2 augmented cancer hallmarks in human HCC cells by binding to the promoters of tumor promoting genes and non-coding RNAs and regulating their transcription. Thus, TAF2 plays a unique and central role in hepatocyte survival and tumorigenesis.
Understanding and mitigating medication errors associated with patient harm in adult intensive care units: a scoping review
Authors: Kathryn Puxty, Margo van Mol, María Cruz Martin Delgado, Michael Darmon, Ricardo Ferrer, Alessandro Galazzi, Entela Kondi, Lene Russell, Elena Sancho, Marlies Ostermann, Elie Azoulay, Richard S Bourne
Journal: Intensive Care Medicine (2025)