Background: This study was performed to assess the effect of poly-N-acetyl glucosamine fiber slurry on plasma clotting proteins, platelets, and red blood cells in the clotting of the blood.
Methods: Citrate phosphate dextrose whole blood was stored at 22degreesC for 48 hours to prepare platelet-poor plasma, platelet-rich plasma (PRP), and PRP plus red blood cells with hematocrit values of 20%, 35%, and 45% with and without an equal volume of poly-N-acetyl glucosamine fibers (1 mg/mL 0.9% NaCl).
Results: Thromboelastogram data show that poly-N-acetyl glucosamine fibers (p-GlcNAc) significantly reduced the R time in platelet-poor plasma, PRP, and PRP supplemented with red blood cells. Poly-N-acetyl glucosamine fibers increased, but not significantly, Annexin V and factor X binding to platelets, platelet microparticles, and red blood cell Annexin V binding. Poly-N-acetyl glucosamine fibers increased the production of thromboxane B2 by PRP.
Conclusion: Poly-N-acetyl glucosamine slurry activates platelets.
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http://dx.doi.org/10.1097/01.ta.0000136744.12440.47 | DOI Listing |
Cell Chem Biol
December 2024
Chemical Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. Electronic address:
Polysaccharide intercellular adhesin (PIA), an exopolysaccharide composed of poly-N-acetyl glucosamine (PNAG), is an essential component in many pathogenic biofilms. Partial deacetylation of PNAG is required for biofilm formation, but limited structural knowledge hinders therapeutic development. Employing a new monoclonal antibody (TG10) that selectively binds highly deacetylated PNAG and an antibody (F598) in clinical trials that binds highly acetylated PNAG, we demonstrate that PIA within the biofilm contains distinct regions of highly acetylated and deacetylated exopolysaccharide, contrary to the previous model invoking stochastic deacetylation throughout the biofilm.
View Article and Find Full Text PDFNat Commun
April 2024
Department of Chemistry, Michigan State University, 578 S. Shaw Lane, East Lansing, MI, 48824, USA.
Poly-β-(1-6)-N-acetylglucosamine (PNAG) is an important vaccine target, expressed on many pathogens. A critical hurdle in developing PNAG based vaccine is that the impacts of the number and the position of free amine vs N-acetylation on its antigenicity are not well understood. In this work, a divergent strategy is developed to synthesize a comprehensive library of 32 PNAG pentasaccharides.
View Article and Find Full Text PDFJ Oral Microbiol
January 2024
Stomatological Hospital and College, Key Lab. of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei, Anhui, China.
Aims: The current study aimed to explore the adjuvant therapeutic effect of N-acyl homoserine lactones (AHLs)-lactonase est816 on biological behaviors and periodontitis progression.
Methods: The inhibitory properties of est816 were detected by live/dead bacterial staining, scanning electron microscope (SEM), crystal-violet staining and reverse-transcription quantitative PCR (RT-qPCR). Biocompatibility of est816 on human gingival fibroblasts (HGFs) and human gingival epithelial cells (HGEs) was evaluated by CCK8 and ELISA.
NPJ Biofilms Microbiomes
December 2023
Department of Molecular Biology and Umeå Centre for Microbial Research (UCMR), Umeå University, SE-90187, Umeå, Sweden.
Acinetobacter baumannii has emerged as one of the most common extensive drug-resistant nosocomial bacterial pathogens. Not only can the bacteria survive in hospital settings for long periods, but they are also able to resist adverse conditions. However, underlying regulatory mechanisms that allow A.
View Article and Find Full Text PDFMicroorganisms
August 2023
Feed Research Institute, Chinese Academy of Agricultural Sciences, Beijing 100081, China.
Rhamnolipid (RL) can inhibit biofilm formation of O157:H7, but the associated mechanism remains unknown. We here conducted comparative physiological and transcriptomic analyses of cultures treated with RL and untreated cultures to elucidate a potential mechanism by which RL may inhibit biofilm formation in O157:H7. Anti-biofilm assays showed that over 70% of the O157:H7 biofilm formation capacity was inhibited by treatment with 0.
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