tbuckley/cabot-search huggingface dataset:
Spreading the reduction of fear: A narrative review on generalization of extinction learning in human fear conditioning
Authors: Alex H K Wong
Journal: Clinical Psychology Review (2025)

Extinction learning refers to a reduction in fear to a conditioned stimulus (CS) that previously signaled a threat, but now occurs without the expected threat. This mechanism is core to exposure-based treatments for anxiety-related disorders. Enhancing the generalization of extinction learning is crucial for improving treatment outcomes, as it helps reduce fear across a range of generalization stimuli (GSs) resembling the original fear-evoking CS. This narrative review identifies and covers three generalization of extinction learning models: 1) generalization of CS extinction learning, examining how extinction learning to the CS generalizes to novel GSs, 2) generalization of GS extinction learning, assessing how extinction learning to a GS generalizes to other novel GSs or the original CS, and 3) generalization of multiple stimuli extinction learning, where extinction learning involves multiple GSs (and sometimes the CS) and its effect on other novel stimuli. While extinction learning to the CS effectively generalizes to other stimuli, extinction learning to a GS or multiple GSs showed limited generalization to other novel GSs or the original CS. Since real-life exposure-based treatment rarely reproduces the CS, extinction learning involving only the GS(s) may better reflect clinical practice; poor generalization of GS(s) extinction learning may constitute another pathway of return of fear. This review also highlights various factors that influence generalization of extinction learning and call for future research to develop strategies for improving these processes, which can help inform exposure-based treatments.
Finerenone Across the Spectrum of Kidney Risk in Heart Failure: The FINEARTS-HF Trial
Authors: John W Ostrominski, Finnian R Mc Causland, Brian L Claggett, Akshay S Desai, Pardeep S Jhund, Carolyn S P Lam, Michele Senni, Sanjiv J Shah, Adriaan A Voors, Faiez Zannad, Bertram Pitt, Patrick Schloemer, Meike Brinker, Markus F Scheerer, John J V McMurray, Scott D Solomon, Muthiah Vaduganathan
Journal: JACC Heart Failure (2025)
Initial Experience With Aeson Total Artificial Heart in Cardiogenic Shock Patients on Extracorporeal Life Support
Authors: Anne-Céline Martin, Mouhamed D Moussa, Bernd Panholzer, Alessandro Verde, Julien Guihaire, Hug Aubin, Alexey Dashkevich, Johannes Kroll, Alexandre Mebazaa, Marco Metra, Federico Pappalardo
Journal: JACC Heart Failure (2025)
Finerenone and New York Heart Association Functional Class in Heart Failure: The FINEARTS-HF Trial
Authors: John W Ostrominski, Muthiah Vaduganathan, Brian L Claggett, Akshay S Desai, Pardeep S Jhund, Carolyn S P Lam, Michele Senni, Sanjiv J Shah, Adriaan A Voors, Faiez Zannad, Bertram Pitt, Maria Borentian, Katja Rohwedder, James Lay-Flurrie, Marco Antonio Lavagnino, John J V McMurray, Scott D Solomon
Journal: JACC Heart Failure (2025)

The NYHA functional classification remains an important and widely used metric in heart failure (HF)-oriented clinical care and research. This study aims to evaluate whether the effect of finerenone varies according to NYHA functional class in HF with mildly reduced or preserved ejection fraction. In this prespecified analysis of the FINEARTS-HF trial, treatment effects of finerenone according to baseline NYHA functional class (II or III/IV) were examined on the primary endpoint (cardiovascular death and total HF events) and key secondary endpoints. Effects of finerenone on change in NYHA functional class were evaluated using ordinal logistic regression. At baseline, 4,146 (69%) and 1,854 (31%) participants were NYHA functional class II and III/IV, respectively. Participants with baseline NYHA functional class III/IV vs II experienced a significantly higher rate of cardiovascular death and total HF events (adjusted rate ratio: 1.28 [95% CI: 1.11-1.46]; P < 0.001). Finerenone consistently reduced the primary endpoint irrespective of baseline NYHA functional class (Pinteraction = 0.54), with greater absolute benefits in NYHA functional class III/IV (absolute rate reduction [ARR]: 4.5 per 100 person-years) vs II (ARR: 2.0 per 100 person-years). Benefits of finerenone on Kansas City Cardiomyopathy Questionnaire-Total Symptom Score at 12 months were consistent irrespective of NYHA functional class (Pinteraction = 0.93). NYHA functional class improved similarly in the finerenone and placebo arms out to 12 months. The safety profile of finerenone was similar among participants with baseline NYHA functional class III/IV vs II. In this FINEARTS-HF analysis, finerenone reduced clinical outcomes and improved patient-reported health status in HF with mildly reduced or preserved ejection fraction irrespective of baseline NYHA functional class. (Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients with Heart Failure [FINEARTS-HF]; NCT04435626).
Cardiopulmonary Exercise Testing With Exercise Echocardiography to Assess Treatment Response in Transthyretin Amyloid Cardiomyopathy
Authors: Rishi K Patel, Francesco Bandera, Lucia Venneri, Daniel Knight, Aldostefano Porcari, Vivek Muthurangu, Marco Guazzi, Philip N Hawkins, Julian D Gillmore, Marianna Fontana
Journal: JACC Heart Failure (2025)
Devices to overcome the buccal mucosal barrier to administer Therapeutic Peptides
Authors: Sahil Malhotra, Thomas Lijnse, Eoin O' Cearbhaill, David J Brayden
Journal: Advanced Drug Delivery Reviews (2025)

Peptide therapeutics are important in healthcare owing to their high target specificity, therapeutic efficacy, and relatively low side effect profile. Injections of these agents have improved thetreatment of chronic diseases including autoimmune, metabolic disorders, and cancer. However, their administration via injections can prove a barrier to patient acceptability of treatments. While oral delivery of these molecules is preferable, oral peptide formulations are associated with limited bioavailability due to degradation in the intestine and low epithelial permeability. Buccal administration of peptides is a potential alternative to injections and oral formulations. Similar to the oral route, the buccal route can promote better patient adherence to dosing regimens, along with the added advantages of not requiring restriction on food or drink consumption before and after administration, as well as avoidance of the liver first-pass metabolism. However, like oral, effective buccal absorption of peptides is still challenging due to the high epithelial permeability barrier. We present a multidisciplinary approach to understanding the buccal physiological barrier to macromolecule permeation and discuss how engineered devices may overcome it. Selected examples of buccal devices can facilitate fast and efficient macromolecule absorption through multiple mechanisms including physical disruption of epithelia, convection-based mass transfer, and a combination of physicochemical strategies. Importantly, minimally invasive devices can be self-applied and are associated with the maintenance of the barrier after exposure. We analysed the critical attributes that are required forthe clinical translation of buccal peptide administration devices. These include performance-driven device development, manufacturing features, patient acceptability, and commercial viability.
Clearance of Senescent Vascular Smooth Muscle Cells Retards Aging-related Restenosis following Bioresorbable Scaffolds Implantation
Authors: Yang Wang, Hang Zou, Zhufeng Dong, Wen Shi, Junyang Huang, Miaolong Yang, Xiaoqing Xiang, Li Xiaotong, Liu Zhifeng, Guixue Wang, Yazhou Wang, Tieying Yin
Journal: Biomaterials (2025)
Enhance the transparency in the development of the BAD living guidelines
Authors: Hui Liu, Yuanyuan Yao, Yaolong Chen
Journal: British Journal of Dermatology (2025)

After the concept of living guidelines was proposed, BAD began to use this methodology and published two living guidelines related to Behçets and alopecia areata. We read and studied these two guidelines with great interest, especially the methodological section; however, we found that there is still room for improvement in several aspects of transparency in their development.
Molecular pathways and diagnosis in spatially resolved Alzheimer’s hippocampal atlas
Authors: Pan Wang, Lei Han, Lifang Wang, Quyuan Tao, Zhen Guo, Ting Luo, Youzhe He, Zhi Xu, Jiayi Yu, Yuyang Liu, Zihan Wu, Bin Xu, Bufan Jin, Yanrong Wei, Ying Yang, Mengnan Cheng, Yujia Jiang, Chen Tian, Huiwen Zheng, Zhongqin Fan, Peiran Jiang, Yue Gao, Juanli Wu, Shengpeng Wang, Bing Sun, Zheng Fang, Junjie Lei, Benyan Luo, Huiying Wen, Guoping Peng, Yuanchun Tang, Tao Yang, Jing Chen, Zhenkun Zhuang, Xinhui Su, Catherine Pan, Keqing Zhu, Yi Shen, Shiping Liu, Aimin Bao, Jianhua Yao, Jian Wang, Xun Xu, Xiao-Ming Li, Longqi Liu, Shumin Duan, Jing Zhang
Journal: Neuron (2025)
Ceramide-induced FGF13 impairs systemic metabolic health
Authors: Jamal Naderi, Amanda Kelsey Johnson, Himani Thakkar, Bhawna Chandravanshi, Alec Ksiazek, Ajay Anand, Vinnyfred Vincent, Aaron Tran, Anish Kalimireddy, Pratibha Singh, Ayushi Sood, Aasthika Das, Chad Lamar Talbot, Isabella A Distefano, J Alan Maschek, James Cox, Ying Li, Scott A Summers, Donald J Atkinson, Tursun Turapov, Jason A Ratcliff, Javis Fung, Asim Shabbir, M Shabeer Yassin, Sue-Anne Toh Ee Shiow, William L Holland, Geoffrey S Pitt, Bhagirath Chaurasia
Journal: Cell Metabolism (2025)
Accelerated Molecular Transportation in the Brain ECS with 755 nm Light Attenuates PSCI in Rats
Authors: Liu Yang, Yajuan Gao, Leonor Serrano Lopes, Jingge Lian, Wanyi Fu, Hanbo Tan, Shuangfeng Yang, Zhaoheng Xie, Yixing Huang, Jicong Zhang, Yanye Lu, Hao Tang, Bo Xiong, Xunbin Wei, Lide Xie, Yun Peng, Xinyu Liu, Hongbin Han
Journal: Cyborg and Bionic Systems (2025)

Ischemic stroke exacts a heavy toll in death and disability worldwide. After ischemic stroke, the accumulation of pathobiomolecules in the brain extracellular space (ECS) will exacerbate neurological damage and cognitive impairment. Photobiomodulation (PBM) has been demonstrated to improve cognitive function in Alzheimer's disease mouse models by accelerating molecular transportation in the brain ECS. This suggests that PBM may have a potential role in the accumulation of pathobiomolecules in the brain ECS following ischemic stroke. In this study, we developed a PBM therapy apparatus with custom parameters. By evaluating the treatment effect, we identified that 755 nm was the optimal light wavelength for ischemic stroke in rats with transient middle cerebral artery occlusion/reperfusion. Extracellular diffusion and interstitial fluid (ISF) drainage were measured using a tracer-based magnetic resonance imaging method. Our results showed that PBM accelerated molecular transportation in the brain ECS and ISF drainage, promoting the clearance of pro-inflammatory cytokines and reducing the deposition of pathological proteins. Consequently, the infarct volume decreased and neurological cognitive function was improved. Besides, the acceleration of ISF drainage was achieved by reducing expression and restoring polarization of aquaporin 4 (AQP4) in the peri-infarct area. In summary, we demonstrated that PBM could alleviate ischemia-reperfusion injury and prevent post-stroke cognitive impairment by accelerating molecular transportation in the brain ECS, paving a pathway for ischemic stroke treatment via the light-ECS interaction.
TIMEPOINT, a phase 1 study combining MTL-CEBPA with pembrolizumab, supports the immunomodulatory effect of MTL-CEBPA in solid tumors
Authors: Ruth Plummer, Mikael H Sodergren, Rose Hodgson, Bríd M Ryan, Nina Raulf, Joanna P Nicholls, Vikash Reebye, Jon Voutila, Laura Sinigaglia, Tim Meyer, David J Pinato, Debashis Sarker, Bristi Basu, Sarah Blagden, Natalie Cook, Thomas R Jeffrey Evans, Jeffrey Yachnin, Cheng E Chee, Daneng Li, Anthony El-Khoueiry, Maria Diab, Kai-Wen Huang, Madhava Pai, Duncan Spalding, Thomas Talbot, Marcus S Noel, Bridget Keenan, Devalingam Mahalingam, Min-Sun Song, Mélanie Grosso, Denis Arnaud, Aurelie Auguste, Dimitris Zacharoulis, Jan Storkholm, Iain McNeish, Robert Habib, John J Rossi, Nagy A Habib
Journal: Cell Reports Medicine (2025)

Many patients with cancer do not benefit from currently approved immune checkpoint inhibitors (ICIs), suggesting that additional immunomodulation of the immunosuppressive tumor microenvironment (TME) is required. MTL-CCAAT enhancer-binding protein alpha (CEBPA) specifically upregulates the expression of the master myeloid transcription factor, CEBPA, relieving myeloid-driven immunosuppression. Here, we report the safety, tolerability, pharmacokinetics, and efficacy of MTL-CEBPA in combination with pembrolizumab in patients with advanced solid tumors that typically show ICI resistance. Multimodal exploratory analyses of paired patient biopsies demonstrate biological changes associated with the combination treatment of MTL-CEBPA and pembrolizumab, including increased infiltration of T cell and antigen-presenting cells supporting conversion from an immune-desert toward a more immune-inflamed TME. Patients with disease stabilization demonstrate reductions in immunosuppressive myeloid cells post treatment. Collectively, these data support a role for MTL-CEBPA in reducing immunosuppression in the TME. This study was registered at ClinicalTrials.gov (NCT04105335).
Highly potent quinoxalinediones inhibit α-hemolysin and ameliorate Staphylococcus aureus lung infections
Authors: Aditya Shekhar, Raffaella Di Lucrezia, Karoline Jerye, Vadim S Korotkov, Kirsten Harmrolfs, Katharina Rox, Herbert A Weich, Ishan Ghai, Florent Delhommel, Isabelle Becher, Carsten Degenhart, Eyad Fansa, Anke Unger, Peter Habenberger, Bert Klebl, Peer Lukat, Stefan Schmelz, Steffi Henke, Sebastian Borgert, Julia C Lang, Florenz Sasse, Randi Diestel, Clémentine Richter, Nicole Schneider-Daum, Bettina Hinkelmann, Jana Niemz, Claus-Michael Lehr, Lothar Jänsch, Jochen Huehn, Richard Alm, Mikhail Savitski, Tobias Welte, Thomas Hesterkamp, Michael Sattler, Mathias Winterhalter, Wulf Blankenfeldt, Eva Medina, Ursula Bilitewski, Klaus Dinkel, Mark Brönstrup
Journal: Cell Host & Microbe (2025)
Diverse priming outcomes under conditions of very rare precursor B cells
Authors: Patrick J Madden, Ester Marina-Zárate, Kristen A Rodrigues, Jon M Steichen, Monolina Shil, Kaiyuan Ni, Katarzyna Kaczmarek Michaels, Laura Maiorino, Amit A Upadhyay, Swati Saha, Arpan Pradhan, Oleksandr Kalyuzhiny, Alessia Liguori, Paul G Lopez, Ivy Phung, Claudia Flynn, Amelia Zhou, Mariane B Melo, Ashley Lemnios, Nicole Phelps, Erik Georgeson, Nushin Alavi, Michael Kubitz, Danny Lu, Saman Eskandarzadeh, Amanda Metz, Oscar L Rodriguez, Kaitlyn Shields, Steven Schultze, Melissa L Smith, Brandon S Healy, Deuk Lim, Vanessa R Lewis, Elana Ben-Akiva, William Pinney, Justin Gregory, Shuhao Xiao, Diane G Carnathan, Sudhir Pai Kasturi, Corey T Watson, Steven E Bosinger, Guido Silvestri, William R Schief, Darrell J Irvine, Shane Crotty
Journal: Immunity (2025)
Sequential membrane- and protein-bound organelles compartmentalize genomes during phage infection
Authors: Emily G Armbruster, Phoolwanti Rani, Jina Lee, Niklas Klusch, Joshua Hutchings, Lizbeth Y Hoffman, Hannah Buschkaemper, Eray Enustun, Benjamin A Adler, Koe Inlow, Arica R VanderWal, Madelynn Y Hoffman, Daksh Daksh, Ann Aindow, Amar Deep, Zaida K Rodriguez, Chase J Morgan, Majid Ghassemian, Thomas G Laughlin, Emeric Charles, Brady F Cress, David F Savage, Jennifer A Doudna, Kit Pogliano, Kevin D Corbett, Elizabeth Villa, Joe Pogliano
Journal: Cell Host & Microbe (2025)
The Cardiovascular Care of the Pediatric Athlete
Authors: Peter N Dean, Julie A Brothers, Kristin Burns, Jonathan B Edelson, Susan Etheridge, Dermot M Phelan, Keri Shafer, Chris Snyder, Silvana Molossi, Alfred Danielian, Eli M Friedman, Jeff Hsu, Mustafa Husaini, Eugene H Chung, Matthew W Martinez, Aaron L Baggish, Benjamin D Levine, Jonathan H Kim
Journal: Journal of the American College of Cardiology (2025)
New Threshold for Defining Mild Aortic Stenosis Derived From Velocity-Encoded MRI in 60,000 Individuals
Authors: Shinwan Kany, Joel T Rämö, David Playford, Geoff Strange, Cody Hou, Sean J Jurgens, Victor Nauffal, Jonathan W Cunningham, Emily S Lau, Atul J Butte, Jennifer E Ho, Jeffrey E Olgin, Sammy Elmariah, Mark E Lindsay, Yih-Kai Chan, Simon Stewart, Patrick T Ellinor, James P Pirruccello
Journal: Journal of the American College of Cardiology (2025)
PCSK9 Regulates Cardiac Mitochondrial Cholesterol by Promoting TSPO Degradation
Authors: Marion Laudette, Malin Lindbom, Mathieu Cinato, Per-Olof Bergh, Kristina Skålén, Arif Muhammad, Azra Miljanovic, Tomasz Czuba, Rosie Perkins, J. Gustav Smith, Frank Lezoualc'h, Malin C. Levin, Jan Borén
Journal: Circulation Research (2025)

BACKGROUND: Cholesterol is critical for mitochondrial membrane structure and function. Given the emergence of mitochondria as a key factor in the pathogenesis of heart failure, mitochondrial cholesterol homeostasis may be crucial for maintaining mitochondrial properties and thus cardiac function. We previously showed that CM- Pcsk9 –/– mice (mice with cardiomyocyte-specific deletion of PCSK9 [proprotein convertase subtilisin-kexin type 9]) have impaired cardiomyocyte mitochondrial bioenergetics and heart function, paralleled by cardiomyocyte mitochondrial cholesterol accumulation and an increased number of mitochondria–endoplasmic reticulum contacts. However, the mechanisms linking PCSK9 to mitochondrial cholesterol homeostasis remain unclear. We hypothesized that PCSK9 acts on proteins involved in mitochondrial cholesterol trafficking in the heart to maintain cardiac mitochondrial function. METHODS: By performing RNA sequencing and immunoblot on CM- Pcsk9 –/– and CM- Pcsk9 +/+ mouse hearts, we showed that TSPO (translocator protein) was increased by Pcsk9 deficiency. To investigate the relationship between TSPO levels and heart function in humans, we compared the transcriptome of human left ventricles with high versus low TSPO levels. We used H9c2 (a rat cardiomyoblast cell line) cardiomyocytes to explore the mechanism linking PCSK9/TSPO to mitochondrial cholesterol content and function. The impact of reduced TSPO levels on cardiac function and mitochondrial oxidation in CM- Pcsk9 –/– mice was tested using adeno-associated virus serotype 9 short hairpin TSPO. RESULTS: Both gene and protein levels of TSPO, a mitochondrial protein involved in cholesterol transport, were increased in CM- Pcsk9 –/– mouse hearts. Transcriptome analysis showed that high TSPO expression in human left ventricles was associated with impaired mitochondrial and cardiac function. We showed that PCSK9 induced TSPO degradation through a proteasomal mechanism that occurs in cardiomyocytes but not hepatocytes and contributes to maintaining normal mitochondrial cholesterol composition and function. At the molecular level, endoplasmic reticulum–resident PCSK9 interacted with GRP78, reducing GRP78-TSPO interactions and leading to TSPO misfolding and degradation by the ubiquitin-proteasome pathway. Importantly, gene therapy–induced downregulation of TSPO in CM- Pcsk9 − / − mice prevented mitochondrial cholesterol accumulation and improved cardiac function. CONCLUSIONS: These findings indicate that PCSK9 regulates mitochondrial cholesterol levels by modulating the TSPO degradation in the heart. Modulation of mitochondrial cholesterol by targeting TSPO may be a promising therapeutic approach for heart failure.
Sirt5 regulates chondrocyte metabolism and osteoarthritis development through protein lysine malonylation
Authors: Huanhuan Liu, Anupama Binoy, Siqi Ren, Thomas C. Martino, Anna E. Miller, Craig R. G. Willis, Shivakumar R. Veerabhadraiah, Joanna Bons, Jacob P. Rose, Birgit Schilling, Michael J. Jurynec, Shouan Zhu
Journal: Arthritis & Rheumatology (2025)

Objectives Chondrocyte metabolic dysfunction plays an important role in osteoarthritis (OA) development during aging and obesity. Protein post‐translational modifications (PTMs) have recently emerged as an important regulator of cellular metabolism. We aim to study one type of PTM, lysine malonylation (MaK) and its regulator Sirt5 in OA development. Methods Human and mouse cartilage tissues were used to measure SIRT5 and MaK levels. Both systemic and cartilage‐specific conditional knockout mouse models were subject to high‐fat diet (HFD) treatment to induce obesity and OA. Proteomics analysis was performed in Sirt5 ‐/‐ and WT chondrocytes. SIRT5 mutation was identified in the Utah Population Database (UPDB). Results We found that SIRT5 decreases while MAK increases in the cartilage during aging. A combination of Sirt5 deficiency and obesity exacerbates joint degeneration in a sex dependent manner in mice. We further delineate the malonylome in chondrocytes, pinpointing MaK's predominant impact on various metabolic pathways such as carbon metabolism and glycolysis. Lastly, we identified a rare coding mutation in SIRT5 that dominantly segregates in a family with OA. The mutation results in substitution of an evolutionally invariant phenylalanine (Phe–F) to leucine (Leu–L) (F101L) in the catalytic domain. The mutant protein results in higher MaK level and decreased expression of cartilage ECM genes and upregulation of inflammation associated genes. Conclusions We found that Sirt5 mediated MaK is an important regulator of chondrocyte cellular metabolism and dysregulation of Sirt5‐MaK could be an important mechanism underlying aging and obesity associated OA development. image
Anti‐Peptidylarginine‐4 Autoantibodies Derived from Patients with Rheumatoid Arthritis Exert Pathogenic Effects by Activating Monocytes and Exacerbating Inflammatory Arthritis
Authors: Taejoon Won, Pooja Naik, Megan K. Wood, Hong Wang, Monica V. Talor, Jing Shi, William Bracamonte‐Baran, Mekha A. Thomas, Camille M. Jaime, Wonyoung Jo, Shreyanshu Ray, Catherine A. Foss, Felipe Andrade, Daniela Čiháková, Erika Darrah
Journal: Arthritis & Rheumatology (2025)

Objective Autoantibodies targeting peptidylarginine deiminase 4 (PAD4), an enzyme involved in protein citrullination, are found in a subset of rheumatoid arthritis (RA) patients with severe joint disease. However, the mechanisms by which anti‐PAD4 antibodies participate in disease pathogenesis are incompletely defined. Methods We investigated the role of anti‐PAD4 monoclonal antibodies derived from RA patients using a collagen‐induced arthritis (CIA) mouse model and human monocyte in vitro cultures. The cellular targets of anti‐PAD4 antibodies were identified using mouse knee joint cells and human peripheral blood mononuclear cells (PBMC). In addition, PAD4 gene and protein expression were assessed using human fibroblast‐like synoviocyte in vitro cultures and a single‐cell RNA sequencing dataset obtained from RA patients. Results We show that anti‐PAD4 antibody treatment augmented disease severity in the CIA mouse model, with increased joint damage, myeloid cell infiltration, and synovial fibroblast activation. Arthritic mice administered with anti‐PAD4 antibodies had an increased proportion of IL‐17A, TNF‐α, and IFN‐γ‐producing T cells . Anti‐PAD4 antibodies preferentially bound monocytes in both humans and mice, eliciting pro‐inflammatory chemokine production by human monocytes in vitro . T cell cytokines enhanced by anti‐PAD4 antibodies in the CIA model, i.e. IL‐17A, TNF‐α, and IFN‐γ, synergized to induce a pro‐inflammatory phenotype in human fibroblast‐like synoviocytes. Conclusion Our findings suggest a model in which anti‐PAD4 antibody binding to monocytes triggers an inflammatory cascade that promotes immune cell recruitment to the joint and T cell activation, culminating in synovial fibroblast activation and the development of more severe arthritis. image
The intersection of socioeconomic deprivation and antimicrobial resistance: refocusing on a key determinant
Authors: Akaninyene Otu, Vinesh Patel, Stuart Bond, Sarah Chadwick, Bassey Ebenso, Mamoon Aldeyab, Jade Lee-Milner, Victoria Hemming, Kathyrn Deakin, Maria Marcolin
Journal: The Lancet Microbe (2025)