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Background: Immunoglobulin G antibodies (Abs) to platelet factor 4 (PF4) complexed to heparin (PF4/H) commonly occur after H exposure but cause life-threatening complications of H-induced thrombocytopenia (HIT) in only a few patients. Presently, only platelet activation assays reliably distinguish anti-PF4/H Abs that cause disease (HIT Abs) from those likely to be asymptomatic (AAbs).

Objectives: Recent studies indicate that complement activation is an important serologic property of HIT Abs and is essential for IgG Fc receptor IIA-mediated cellular activation.

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The threats to chemical warfare-associated agents (CWA), including nitrogen mustard, are increasing, and no direct antidote is currently available to mitigate the deleterious cutaneous and systemic responses to prevent mortality. Though most of these agents act as alkylating agents, a significant knowledge gap exists in the molecular mechanisms of how these vesicants cause toxic effects. Studies, including ours, have shown that exposure to reactive oxygen species (ROS)-generating stimuli, including alkylating chemotherapeutic agents, and thermal burn injuries with ethanol produce the potent family of lipid mediators, Platelet-activating factor (PAF) agonists that induce local inflammation, and multi-system organ dysfunction (MOD).

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Role of Platelet-Activating Factor in the Pathogenesis of Chronic Spontaneous Urticaria.

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Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon 16499, Republic of Korea.

Chronic spontaneous urticaria (CSU) is a debilitating condition characterized by mast cell activation. Platelet-activating factor (PAF) is produced by various immune cells, including mast cells, basophils, lymphocytes, and eosinophils, which play crucial roles in CSU pathogenesis. It induces mast cell degranulation, increases vascular permeability, and promotes the chemotaxis of inflammatory cells.

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Mounting evidence strongly indicates that exosomes are pivotal in the advancement of cancer, yet the overarching profile of exosomal proteins and their contribution to lung adenocarcinoma (LUAD) progression remain underexplored. In our investigation, we isolated exosomes from treatment-naive LUAD (n = 20) and paired normal adjacent tissues (NATs), and conducted integrated proteomic on the acquired exosomes and source tissues to ascertain origin characteristics and potential therapeutic targets of the exosomal proteins in LUAD. The omics data revealed the overall landscape of exosomal proteins from tissues in LUAD, underscoring the profound linkage between exosomal proteins and tumor metastasis.

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Article Synopsis
  • * The treatment strategy combined high-dose intravenous immunoglobulin (IVIG) and high concentrations of heparin to lessen the risk of platelet activation during surgery.
  • * Results showed that preoperative IVIG significantly reduced platelet activation, allowing the safe use of standard heparin during the surgery without causing thrombosis.
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