tbuckley/cabot-search huggingface dataset:
On the conversational persuasiveness of GPT-4
Authors: Francesco Salvi, Manoel Horta Ribeiro, Riccardo Gallotti, Robert West
Journal: Nature Human Behaviour (2025)

Abstract Early work has found that large language models (LLMs) can generate persuasive content. However, evidence on whether they can also personalize arguments to individual attributes remains limited, despite being crucial for assessing misuse. This preregistered study examines AI-driven persuasion in a controlled setting, where participants engaged in short multiround debates. Participants were randomly assigned to 1 of 12 conditions in a 2 × 2 × 3 design: (1) human or GPT-4 debate opponent; (2) opponent with or without access to sociodemographic participant data; (3) debate topic of low, medium or high opinion strength. In debate pairs where AI and humans were not equally persuasive, GPT-4 with personalization was more persuasive 64.4% of the time (81.2% relative increase in odds of higher post-debate agreement; 95% confidence interval [+26.0%, +160.7%], P &lt; 0.01; N = 900). Our findings highlight the power of LLM-based persuasion and have implications for the governance and design of online platforms.
The impact of non-steroidal anti-inflammatory drugs on postoperative bleeding in children undergoing tonsillectomy: a meta-analysis of randomized controlled trials
Authors: Yue Lu, Bo Feng, Ling-Hui Guo, Qiong-Yu Wu, Yu-Zhen Zhang, Min-Xiao Li, Xiao-Gang Chen, Meng-Sha Nie, Na Li, Run-Wei Ma, Li-Ming Cheng
Journal: International Journal of Surgery (2025)
Adaptation to Volumetric Compression Drives an Apoptosis-Resistant and Invasive Phenotype in Liver Cancer
Authors: Xiangyu Gong, Noriyoshi Ogino, M. Fátima Leite, Dingyao Zhang, Zehua Chen, Ryan Y. Nguyen, Raymond Liu, Emma Kruglov, Kaitlin Flores, Aidan T. Cabral, Gabriel Moreira de M. Mendes, Barbara E. Ehrlich, Michael Mak
Journal: Cancer Research (2025)

Abstract Physical constraints like compression influence cancer cell invasion and transcriptional dynamics in various tumors. Liver cancer is characterized by the rapid proliferation of tumor cells within a densely packed tissue matrix, subjecting the cancer cells to crowding and compression. The highly dysregulated mechanical environment highlights the need to elucidate the broader impact of compression on liver cancer development and evolution. In this study, we investigated and described a unique adaptive response of liver cells to prolonged compression. Liver cells presented significant transcriptional changes due to compression, including the loss of liver-specific markers and enrichment of epithelial-to-mesenchymal transition genes. Compression elevated Rac1 activity, which promoted cellular protrusions and YAP nuclear translocation and maintained cell viability under mechanical stress. Furthermore, compression disrupted intracellular calcium signaling, leading to resistance to apoptosis. Counteracting the effects of compression by inhibiting Rac1 or manipulating intracellular calcium facilitated death of compression-adapted cells. This study highlights compression as a critical biophysical signal in the tissue microenvironment that can induce cell state transitions and disease-driving phenotypes in the liver.
Early Increase in Serum Transthyretin by Acoramidis Independently Predicts Improved Survival in TTR Amyloid Cardiomyopathy
Authors: Mathew S Maurer, Daniel P Judge, Julian D Gillmore, Pablo Garcia-Pavia, Ahmad Masri, Francesco Cappelli, Kevin M Alexander, Nitasha Sarswat, Martha Grogan, Amrut V Ambardekar, Anique Ducharme, Steen H Poulsen, Kaitlyn Lam, Laura Obici, Prem Soman, Satish Rao, Jean-François Tamby, Adam Castaño, Jonathan C Fox, Brian Adam, Surendhar Reddy Chepyala, Bill Poland, Uma Sinha, Marianna Fontana
Journal: Journal of the American College of Cardiology (2025)
Phenotypic heterogeneity and plasticity in colorectal cancer metastasis
Authors: Samuel Ogden, Nasrine Metic, Ozen Leylek, Elise A Smith, Alison M Berner, Ann-Marie Baker, Imran Uddin, Marta Buzzetti, Marco Gerlinger, Trevor Graham, Hemant M Kocher, Mirjana Efremova
Journal: Cell Genomics (2025)
Quality of vitamin K antagonist treatment during the last year of life
Authors: Chantal Visser, Eva K. Kempers, Jamilla Goedgebuur, Denise Abbel, Sarah J. Aldridge, Adrian Edwards, Michelle Edwards, Geert‐Jan Geersing, Anne Gulbech Ording, Sjef J. C. M. van de Leur, Kate J. Lifford, Isabelle Mahé, Simon P. Mooijaart, Melchior C. Nierman, Johanneke E. A. Portielje, Mette Søgaard, Sebastian Szmit, Nynke M. Wiersma, Simon I. R. Noble, Frederikus A. Klok, Qingui Chen, Suzanne C. Cannegieter, Eric C. T. Geijteman, Marieke J. H. A. Kruip
Journal: HemaSphere (2025)

Abstract Limited data exist on the quality of anticoagulation in patients approaching the end of life. This study evaluated vitamin K antagonist (VKA) anticoagulation control during the last year of life, using nationwide data from Statistics Netherlands, linked to anticoagulation clinics' data and the Netherlands Cancer Registry. We included prevalent VKA users who were hospitalized with a severe medical condition and died between January 1, 2013, and December 31, 2019. Anticoagulation control was assessed using time in therapeutic range (TTR), time above therapeutic range (TAR), and time below therapeutic range (TBR) and the international normalized ratio (INR) variance growth rate (VGR), which reflects INR variability. Anticoagulation control was examined by two approaches: (1) over four intervals (0–12 months, 0–9 months, 0–6 months, and 0–3 months preceding death), and (2) in 3‐month intervals (9–12, 6–9, 3–6, and 0–3 months before death) to describe temporal changes. Among 6874 VKA users in their last year of life (median age 82 [Interquartile range: 76–87] years, 46.9% female), the most prevalent severe medical conditions were heart disease (60.4%), cancer (16.2%), and hip fracture (15.2%). As death approached, TTR and TBR decreased, while TAR and mean VGR increased, particularly in the last 3 months of life. This decline was more pronounced in cancer patients and acenocoumarol users. In conclusion, the quality of VKA anticoagulation declined in the last year of life in severely ill patients, marked by reduced TTR and increased TAR and VGR, suggesting an increased bleeding risk. These findings highlight the importance of reassessing VKA use and considering discontinuation in patients approaching the end of life.
Metabolism in hematology: Technological advances open new perspectives on disease biology and treatment
Authors: Eileen Haring, Joerg M. Buescher, Petya Apostolova
Journal: HemaSphere (2025)

Abstract The term metabolism refers to the multi‐faceted biochemical reactions within a cell or an organism that occur to maintain energy homeostasis, cell growth, and oxidative balance. Cells possess a high metabolic plasticity, allowing them to adapt to the dynamic requirements of their functional state and environment. Deregulated cellular metabolism is a hallmark of many diseases, including benign and malignant hematological conditions. In the last decade, multiple technological innovations in the metabolism field have made in‐depth metabolic analysis broadly applicable. Such studies are shedding new light on normal and malignant hematopoiesis and open avenues to a better understanding of the biology of hematological diseases. In this review, we will first give a brief overview of central metabolic processes. Furthermore, we discuss the most commonly used methods to study metabolism. We begin by elaborating on the use of next‐generation sequencing to detect metabolism‐related genomic mutations and study transcriptional signatures. Furthermore, we discuss methods for measuring protein expression, such as mass spectrometry (MS), flow cytometry, and cytometry time‐of‐flight. Next, we describe the use of nuclear magnetic resonance spectroscopy, MS, and flow cytometry for metabolite quantification. Finally, we highlight functional assays to probe metabolic pathways in real‐time. We illustrate how these technologies and their combination have advanced our understanding of the role of metabolism. Our goal is to provide hematologists with a comprehensive guide to modern techniques in metabolism research, their benefits and disadvantages, and how they guide our understanding of disease and potentially future personalized therapy decisions.
Defining molecular circuits of CD8+ T cell responses in tissues during latent viral infection
Authors: Endi K. Santosa, Jennifer M. Zhang, John C. Sauter, Mariah E. Lee, Brandon D. Ng, Sigrun V. Stulz, Meril Takizawa, Simon Grassmann, Orr-El Weizman, Nicholas M. Adams, Ronan Chaligné, Annette Oxenius, Georg Gasteiger, Colleen M. Lau, Joseph C. Sun
Journal: The Journal of Experimental Medicine (2025)

Latent viral infections rely on a precise coordination of the immune response to control sporadic viral reactivation. CD8+ T cells play a crucial role in controlling viral latency by generating diverse memory responses in an epitope-specific manner. Among these distinct responses, conventional and inflationary memory responses have been described during herpesvirus infections. Using a newly generated TCR transgenic mouse strain, we investigated the transcriptomic and epigenetic remodeling of distinct epitope-specific CD8+ T cells during CMV infection across tissues at both population and single-cell levels. Our findings reveal that whereas the transcriptomic and epigenetic landscapes of conventional and inflationary memory responses diverge in the spleen and liver, these molecular programs converge in the salivary gland, a site of CMV persistence. Thus, we provide evidence that the dynamics of memory CD8+ T cell responses are distinct between tissues.
Nose-to-brain drug delivery: from bench to bedside
Authors: Isabell Drath, Franziska Richter, Malte Feja
Journal: Translational Neurodegeneration (2025)

Abstract There is increasing interest in nose-to-brain delivery as an innovative drug delivery strategy for neurodegenerative disorders such as Parkinson’s or Alzheimer’s disease. The unique anatomy of the nose-brain interface facilitates direct drug transport via the olfactory and trigeminal pathways to the brain, bypassing the blood–brain barrier. Different administration techniques as well as advanced drug formulations like targeted nanoparticles and thermoresponsive systems have been explored to improve the delivery efficiency and the therapeutic efficacy. This review provides an up-to-date perspective on this fast-developing field, and discusses different studies on safety and pharmacokinetic properties. A thorough evaluation of preclinical and clinical studies reveals both promises and challenges of this delivery method, highlighting approved drugs for the treatment of epilepsy and migraine that successfully utilize intranasal routes. The current landscape of research on nose-to-brain delivery is critically discussed, and a rationale is provided for ongoing research to optimize therapeutic strategies.
Erratum: Nonphagocytic activation of NOX2 is implicated in progressive nonalcoholic steatohepatitis during aging
Authors: Joy X. Jiang, Sarah R. Fish, Alexey Tomilov, Yuan Li, Weiguo Fan, Ali Dehnad, David Gae, Suvarthi Das, Gergely Mozes, Gregory W. Charville, Jon Ramsey, Gino Cortopassi, Natalie J. Török
Journal: Hepatology (2025)
Retraction: C-Jun mediates hepatitis C virus hepatocarcinogenesis through signal transducer and activator of transcription 3 and nitric oxide-dependent impairment of oxidative DNA repair
Authors: Keigo Machida, Hidekazu Tsukamoto, Jian-Chang Liu, Yuan-Ping Han, Sugantha Govindarajan, Michael M.C. Lai, Shizuo Akira, Jing-Hsiung James Ou
Journal: Hepatology (2025)
Cystatin C as Biomarker for the Evaluation of Renal Outcome in <scp>AL</scp> Amyloidosis
Authors: Foteini Theodorakakou, Despina Fotiou, Filia Apostolakou, Ioannis Papassotiriou, Vasiliki Spiliopoulou, Ioannis Ntanasis‐Stathopoulos, Panagiotis Malandrakis, Magdalini Migkou, Nikolaos Kanellias, Evangelos Eleutherakis‐Papaiakovou, Erasmia Psimenou, Asimina Papanikolaou, Charikleia Gakiopoulou, Smaragdi Marinaki, Stavroula Giannouli, Maria Gavriatopoulou, Evangelos Terpos, Meletios‐Athanasios Dimopoulos, Efstathios Kastritis
Journal: American Journal of Hematology (2025)

ABSTRACT Cystatin C (CysC) has emerged as a novel and potentially more reliable biomarker for the estimation of glomerular filtration in the general population in patients with various conditions. In AL amyloidosis, the current renal staging system and renal response criteria are based on proteinuria and creatinine‐based eGFR. We explored the prognostic role of CysC and of estimation of eGFR based on CysC‐based equations in a cohort of 195 patients with newly diagnosed AL amyloidosis with renal involvement. Baseline CysC level was strongly and independently associated with progression to dialysis, and CysC levels ≥ 1.9 mg/L can be used in combination with the current renal staging system to identify patients with different risk of progression to dialysis among renal stages 2 and 3. eGFR based on CysC performed at least similarly to eGFR based on creatinine alone (by CKD‐EPI race free formula) and the cutoff of 30 mL/min/1.73 m 2 could better predict progression to dialysis at 2 years. At 6 months landmark, an increase in CysC by ≥ 1 mg/L was associated with higher risk of progression to dialysis (HR: 19.8, 95% CI 6.5–60.5, p &lt; 0.001); a reduction of CysC based eGFR ≥ 30% was also associated with poor renal outcome, with a prognostic performance similar to current renal progression criteria. In conclusion, CysC provides prognostic information regarding the renal outcomes in patients with AL amyloidosis independently of the established biomarkers, but requires further validation.
Classical and Late‐Onset <scp>SOS</scp>/<scp>VOD</scp> After Allogeneic <scp>HSCT</scp>: A Japanese Transplant Registry Analysis
Authors: Kyoko Masuda, Keisuke Kataoka, Masatoshi Sakurai, Yuho Najima, Naonori Harada, Shoko Ukita, Naoyuki Uchida, Noriko Doki, Takahiro Fukuda, Masatsugu Tanaka, Hiroyuki Ohigashi, Jun Ishikawa, Satoshi Yoshihara, Masashi Sawa, Shuichi Ota, Yoshinobu Kanda, Tetsuya Nishida, Makoto Onizuka, Yoshiko Atsuta, Hideki Nakasone, Kimikazu Yakushijin
Journal: American Journal of Hematology (2025)

ABSTRACT Sinusoidal obstruction syndrome/veno‐occlusive disease (SOS/VOD) is a lethal complication of allogeneic hematopoietic stem cell transplantation (allo‐HSCT). According to the 2016 European Society for Blood and Marrow Transplantation criteria, SOS/VOD is classified into classical SOS/VOD and late‐onset SOS/VOD, but their similarities and differences remain unclear. Here we retrospectively investigated the incidence, risk factors, and impact on transplant outcomes of classical and late‐onset SOS/VOD in 16 518 allo‐HSCT recipients using the Japanese nationwide registry data. The cumulative incidences of classical and late‐onset SOS/VOD were 2.5% and 2.2%, with a median onset of 13 and 42 days after transplantation, respectively. Both patients with classical (hazard ratio [HR], 3.45; 95% CI, 3.07–3.87) and late‐onset (HR, 3.98; 95% CI, 3.51–4.51) SOS/VOD had a significantly worse overall survival compared with those without. The risk factors for classical and late‐onset SOS/VOD are different. Hepatic comorbidities, high‐risk diseases, use of melphalan (MEL), and myeloablative conditioning are associated with both types of SOS/VOD. Whereas poor performance status, a prior history of transplantation, and positive hepatitis C virus are associated with only classical SOS/VOD, allo‐HSCT from cord blood or related human leukocyte antigen‐haploidentical donors, use of total body irradiation and busulfan (BU), and tacrolimus‐based graft‐versus‐host disease prophylaxis are associated with only late‐onset SOS/VOD. In particular, the incidence of late‐onset SOS/VOD is much higher in patients receiving both BU‐ and MEL‐containing conditioning regimens. These findings suggest that different monitoring and treatment approaches are necessary for allo‐HSCT recipients at high risk for classical and late‐onset SOS/VOD.
Routine Screening of <i>Strongyloides</i> Among Patients With Lymphoma and Efficacy of Targeted Prophylaxis
Authors: Michele D. Stanchina, Camila Sacher, Yamila Melendez, Pamela Dudkiewicz, Jose F. Camargo, Izidore S. Lossos
Journal: American Journal of Hematology (2025)

A total of 1372 lymphoma patients (980 newly diagnosed and 392 seen in cellular therapy clinic) were screened for Strongyloides serology, detecting IgG in 80 (6%) patients. Only one out of 80 (1.25%) patients diagnosed and treated with ivermectin for Strongyloides developed disseminated strongyloidiasis following chemotherapy treatments, supporting routine screening and prophylaxis in lymphoma patients.
<scp>IFNγ</scp> Signaling Impairs Regulatory B Cell Function Resulting in Worse Control of Esophageal Food Allergy
Authors: Rachel L. Clement, Julie Dilollo, Eric M. Rodríguez‐López, Cleandre M. Guerrier, David A. Hill
Journal: Allergy (2025)

ABSTRACT Background Eosinophilic Esophagitis (EoE) is a chronic food allergy that causes esophageal inflammation and fibrosis and manifests with symptoms of reflux, chest pain, swallowing difficulty, and food impactions. Though the prevalence of EoE is increasing by ~15% each year, our understanding of EoE immunopathology is limited. A noted feature of EoE is the presence of food‐specific IgG4 antibodies in the circulation and esophageal tissue. Production of IgG4 is confined to IL‐10 + B cells (Bregs) in other allergic diseases, suggesting Bregs may be present in EoE. Methods We examined circulating Bregs in patients with EoE milk allergy. In parallel, we performed mechanistic investigations of the role of Bregs in a murine model of food‐antigen‐dependent EoE. Flow cytometry and histologic analyses were used to assess esophageal and draining lymph node immune cells, and in vitro assays were used to evaluate Breg functional capacity. Results Breg frequency was reduced in both EoE milk allergic subjects and an EoE disease model. Murine Breg suppressive capacity was impaired during EoE‐like inflammation. Inducible deletion of Breg‐derived IL‐10 worsened EoE‐like inflammation, while adoptive transfer of IL‐10 sufficient Bregs suppressed DC activation and improved esophageal eosinophilia. IFNγ was sufficient to suppress Breg expansion and IL‐10 production in vitro and contributed to Breg dysfunction and esophageal inflammation in vivo. Conclusion Bregs play an immunoregulatory role during EoE by controlling esophageal eosinophilia but are functionally impaired due to IFNγ‐mediated signaling. These findings have important implications for understanding EoE's etiology and implementing future therapies that target IFNγ.
Antiphospholipid syndrome: an antibody‐mediated disease with emerging therapeutic opportunities
Authors: Thalia G. Newman, Jason S. Knight
Journal: Arthritis & Rheumatology (2025)

Antiphospholipid syndrome (APS) is an autoimmune thrombo‐inflammatory disorder characterized by vascular thrombosis, pregnancy morbidity, and other manifestations driven by antiphospholipid autoantibodies. In this review, we present a clinical case that illustrates some diagnostic and therapeutic challenges in managing severe, relapsing APS manifestations, including microvascular injury and diffuse alveolar hemorrhage. We then discuss recent advances in our understanding of APS pathophysiology, emphasizing the critical role of anti‐beta‐2 glycoprotein I antibodies in triggering cell‐specific inflammatory and thrombotic pathways. Finally, we speculate that achieving definitive disease control will require strategies that eliminate or effectively neutralize these pathogenic antibodies.
Precision Medicine in Pediatric Autoimmunity: Leniolisib Treatment of Childhood‐Onset Lupus Nephritis Due to Activated <scp>PI3K</scp>‐Delta Syndrome (<scp>APDS</scp>)
Authors: Jonathan P. Lim, Mansooreh Ahmadian, Hongyu Du, Christian Rickert, Tusharkanti Ghosh, Fuyong Xing, Angela Minic, Sara A. Johnson, Jason P. Weinman, Nicholas Willard, Clara Lin, Jennifer C. Cooper, Melisha Hanna, Vijaya Knight, Debashis Ghosh, Kimberly R. Jordan, Elena WY Hsieh
Journal: Arthritis & Rheumatology (2025)

Objective To investigate the mechanistic underpinnings and treatment response of lupus nephritis (LN) in activated PI3K‐delta syndrome type 1 (APDS1) using pathway‐specific therapy and advanced spatial proteomics. Method We conducted mechanistic investigation of refractory class V LN in an 18‐year‐old female with genetically confirmed APDS1 (PIK3CD c.3061G&gt;A, p.E1021K mutation). Response to leniolisib, a selective PI3Kδ inhibitor, was evaluated through clinical parameters and flow cytometry of peripheral blood lymphocytes. Kidney tissue immune architecture was characterized using Multiplexed Ion Beam Imaging Time‐of‐Flight Spectrometry (MIBI‐TOF), comparing the APDS1‐LN tissue signature with 12 childhood‐onset LN patients (cLN) and 5 healthy controls (HC). Results Leniolisib treatment normalized hyperactive PI3Kδ signaling, resulting in significant improvements in proteinuria, complement levels, and peripheral edema after failing three years of conventional immunosuppressives. MIBI‐TOF spatial proteomics revealed a distinct tissue‐specific immunopathology with significantly increased proportions of CD8+ T cells (21.6% in APDS1 vs. 12.0% in typical LN, p=0.0410) and M1 macrophages (42.0% in APDS1 vs. 9.0% in typical LN, p=0.1445) clustering around glomeruli with immune complex deposition. This immune signature aligns with the constitutively active PI3Kδ pathway's effect on lymphocyte exhaustion and inflammatory phenotype. Conclusion This investigation advances rheumatology by demonstrating that APDS1‐associated LN displays a specific tissue immune signature and responds to targeted inhibition of the causative molecular pathway. Our findings provide mechanistic insights into genetic drivers of autoimmunity and support pathway‐specific therapeutic approaches for refractory autoimmune manifestations in primary immunodeficiencies. image