Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Ulinastatin is a protease-inhibiting drug with anti-inflammatory and other pharmacological properties. Little is known regarding its role following acute type A aortic dissection (ATAAD) surgery. We perform a randomized controlled trial to investigate the protective effect of ulinastatin against negative inflammatory response and organ dysfunction in ATAAD surgery (PANDA). The primary outcome of mean daily Sequential Organ Failure Assessment (SOFA) score from baseline to 7 days of surgery is 8.80 (SD, 4.11) in the ulinastatin group and 8.61 (SD, 4.47) in the control group (mean difference between groups was 0.04; 95% confidence interval [CI], -0.24 to 0.33; p = 0.765). Systemic inflammatory response syndrome (SIRS) within 7 days of surgery is lower in the ulinastatin group than in the control group (p < 0.001). Additional ulinastatin to standard treatment is likely to reduce SIRS rates instead of preventing organ dysfunction, highlighting the potential importance of the benefits of anti-inflammatory pharmacotherapeutics. The trial is registered on clinicaltrials.org (NCT04711889).
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11866440 | PMC |
| http://dx.doi.org/10.1016/j.xcrm.2024.101888 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
14-3-3 Proteins Negatively Regulate Microglial Activation via Inhibition of the NF-κB Pathway.
J Neurochem
September 2025
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Microglia, the resident immune cells of the central nervous system (CNS), are involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease (AD), Dementia with Lewy Bodies (DLB), and Parkinson's disease (PD). 14-3-3 proteins act as molecular hubs to regulate protein-protein interactions, which are involved in numerous cellular functions, including cellular signaling, protein folding, and apoptosis. We previously revealed decreased 14-3-3 levels in the brains of human subjects with neurodegenerative diseases.
View Article and Find Full Text PDFTRPV1 Suppresses Microglial Inflammatory Activation to Ameliorate Schizophrenia-Associated Behaviors in Maternal Separation Rats.
Schizophr Bull
September 2025
Department of Psychiatry, Central Laboratory, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Background And Hypothesis: Schizophrenia is linked to hippocampal dysfunction and microglial inflammatory activation. Our prior clinical findings revealed significantly reduced transient receptor potential vanilloid 1 (TRPV1) expression in both first-episode and recurrent schizophrenia patients, with levels inversely correlating with symptom severity, implicating TRPV1 dysfunction in disease progression. Preclinical maternal separation (MS) models recapitulate schizophrenia-like behavioral and synaptic deficits, paralleled by hippocampal microglial TRPV1 downregulation.
View Article and Find Full Text PDFA Transformable Nanoplatform Precisely Positions Fibroblast-Like Synoviocytes via FAP-α for Improved Rheumatoid Arthritis Therapy.
Adv Healthc Mater
September 2025
State Key Laboratory of Southwestern Chinese Medicine Resources, College of Modern Chinese Medicine Industry, School of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by joint inflammation, damage, and disability. Activated fibroblast-like synoviocytes (FLSs), abundant in RA synovium, crucially facilitate disease progression. These activated FLSs drive RA pathogenesis by upregulating adhesion molecules, proinflammatory cytokines, chemokines, and major histocompatibility complex class II (MHC-II).
View Article and Find Full Text PDFNature-inspired IL-1 targeted therapy to treat chronic inflammatory diseases.
Mol Ther
September 2025
Department of Medicine, UMass Chan Medical School, Worcester, MA, USA; Department of Genetic and Cellular Medicine, UMass Chan Medical School, Worcester, MA, USA; Horae Gene Therapy Center, UMass Chan Medical School, Worcester, MA, USA; Li Weibo Institute for Rare Diseases Research, UMass Chan Medic
The interleukin (IL)-1 pathway is a key mediator of inflammation and innate immune responses. Its dysregulation contributes to rheumatoid arthritis (RA) and autoinflammatory diseases (AIDs). In this study, we develop a recombinant adeno-associated virus (rAAV)-based gene therapy to deliver an inflammation-inducible, secreted human IL-1 receptor antagonist (sIL-1Ra) as a complementary approach to existing IL-1 blockers.
View Article and Find Full Text PDFBackground: Devoid of a lymphatic system, the central nervous system (CNS) relies primarily on innate immunity for protection. While these immune responses help to fight pathogens, they can also cause irreversible damage because of the CNS's limited regenerative capacity. Therefore, it is crucial to understand which CNS cells contribute to pathogen clearance but in doing so potentially damage surrounding tissue.
View Article and Find Full Text PDF