Publications by authors named "B Nal"

Background: Pain is one of the common postoperative issues that impair recovery and quality of life in patients undergoing coronary artery bypass graft (CABG) surgery. It leads to prolonged recovery and sleep disturbances in patients.

Aim: This study was conducted to examine the effect of eye mask use on sleep quality and pain in patients undergoing CABG surgery.

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  • * Factor H (FH) regulates this system, preventing damage to the body's own cells and has been found to interact with human influenza A viruses (IAVs) through the virus's surface protein, haemagglutinin (HA).
  • * The study shows that FH can affect the entry of certain IAV strains into cells, with varying impacts on viral replication, clearly demonstrating that the interactions between FH and IAV depend on the specific strain involved.
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Gain-of-function mutations in stimulator of interferon gene 1 (STING1) result in STING-associated vasculopathy with onset in infancy (SAVI), a severe autoinflammatory disease. Although elevated type I interferon (IFN) production is thought to be the leading cause of the symptoms observed in patients, STING can induce a set of pathways, which have roles in the onset and severity of SAVI and remain to be elucidated. To this end, we performed a multi-omics comparative analysis of peripheral blood mononuclear cells (PBMCs) and plasma from SAVI patients and healthy controls, combined with a dataset of healthy PBMCs treated with IFN-β.

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Endo-lysosomes transport along microtubules and clustering in the perinuclear area are two necessary steps for microbes to activate specialized phagocyte functions. We report that RUN and FYVE domain-containing protein 3 (RUFY3) exists as two alternative isoforms distinguishable by the presence of a C-terminal FYVE domain and by their affinity for phosphatidylinositol 3-phosphate on endosomal membranes. The FYVE domain-bearing isoform (iRUFY3) is preferentially expressed in primary immune cells and up-regulated upon activation by microbes and Interferons.

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  • C4b Binding Protein (C4BP) inhibits the complement system by binding to activated component C4b, working alongside factor I to prevent the formation of the C3-convertase, which is essential for immune response.
  • The study investigates C4BP's ability to interact with Influenza A Virus (IAV) subtypes H1N1 and H3N2, discovering that C4BP binds to various viral proteins and affects infection rates differently for each subtype.
  • C4BP decreases inflammatory responses for H1N1, acting as an entry inhibitor, while it enhances pro-inflammatory responses for H3N2, suggesting that C4BP has strain-dependent effects on IAV entry and replication independent of its
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