Lipopolysaccharide (LPS, endotoxin) is a component of Gram-negative bacteria and is the principal indicator to the innate immune systems of higher animals of a Gram-negative bacterial invasion. LPS activates the blood clotting system of the American horseshoe crab, Limulus polyphemus. By stimulating blood cell degranulation, LPS triggers the release of the proteins of the clotting system from the cells, and by activating a protease cascade that converts coagulogen, a soluble zymogen, to coagulin, the structural protein of the clot, LPS triggers the production of the fibrillar coagulin blood clot. Although originally thought to be restricted to the Gram-negative bacteria and the cyanobacteria, LPS, or a very similar molecule, has recently been described from a eukaryotic green alga, Chlorella. Here we show that, like LPS from Gram-negative bacteria, the algal molecule stimulates exocytosis of the Limulus blood cell and the clotting of coagulin. The coagulin clot efficiently entraps the cells of Chlorella in a network of fibrils. Invasion and erosion of the carapace by green algae is an important cause of mortality of Limulus, and it is suggested that the cellular response to aLPS may contribute to defense against this pathogen.
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http://dx.doi.org/10.1016/j.cbpa.2006.03.013 | DOI Listing |
Behav Brain Res
January 2025
Department of Psychiatry, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China; Department of Psychiatry and Institute of Neuropsychiatry, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei, PR China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, 430071, China. Electronic address:
Background: The global burden of major depressive disorder (MDD) is rising, with current diagnostic methods hindered by significant subjectivity and low inter-rater reliability. Several studies have implied underlying link between coagulation-related proteins, such as kininogen (KNG) and coagulation factor VIII (FVIII), and depressive symptoms, offering new insights into the exploration of depression biomarkers. This study aims to elucidate the roles of KNG and FVIII in depression, potentially providing a foundational basis for biomarker research in this field.
View Article and Find Full Text PDFCureus
December 2024
Department of Colorectal Surgery, Liverpool Hospital, Sydney, AUS.
Blunt abdominal trauma frequently results in visceral injury to either solid or hollow organs; however, injury to the gallbladder is rare. This is most likely due to the anatomical position of the gallbladder, which is well-insulated posterior to the liver and rib cage. Gallbladder injuries can be in the form of avulsion, contusion, or laceration.
View Article and Find Full Text PDFShock
January 2025
Pharmacology, University of Vermont, Burlington, VT.
Objective: Loss of function of the phospholipid scramblase (PLS) TMEM16F results in Scott Syndrome, a hereditary bleeding disorder generally attributed to intrinsic platelet dysfunction. The role of TMEM16F in endothelial cells, however, is not well understood. We sought to test the hypothesis that endothelial TMEM16F contributes to hemostasis by measuring bleeding time and venous clotting in endothelial-specific knockout (ECKO) mice.
View Article and Find Full Text PDFFuture Cardiol
January 2025
Echocardiography research Center, Rajaie cardiovascular medical and research Center, Iran University of Medical Science, Tehran, Iran.
Introduction: Decreased left atrial appendage emptying velocity (LAAV) is a marker for thrombus formation. This study evaluates the association between LAAV and inflammatory indices in non-valvular atrial fibrillation (AF) patients.
Methods: The study population was 1428 patients with AF, 875 of whom enrolled.
Bioconjug Chem
January 2025
Department of Pharmacology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-5127, United States.
Red blood cells (RBCs) serve as natural transporters and can be modified to enhance the pharmacokinetics and pharmacodynamics of a protein cargo. Affinity targeting of Factor IX (FIX) to the RBC membrane is a promising approach to improve the (pro)enzyme's pharmacokinetics. For RBC targeting, purified human FIX was conjugated to the anti-mouse glycophorin A monoclonal antibody Ter119.
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