Publications by authors named "T Rusak"

Neutrophilic pulmonary inflammation in asthmatics substantially exacerbates the severity of the disease leading to resistance to conventional corticosteroid therapy. Many studies established the involvement of Th1- and Th17-cells and cytokines produced by them (IFNg, IL-17A, IL-17F etc.) in neutrophilic pulmonary inflammation.

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  • Adrenaline triggers the exposure of phosphatidylserine (PS) on blood platelets, enhancing the coagulation process, but the underlying mechanism needs further research.
  • Experiments using receptor antagonists and signaling modulators showed that blocking sodium and calcium ion influx significantly reduces PS exposure, while other inhibitors had a moderate effect.
  • The study highlights the key roles of ion exchangers, ADP signaling, GPIIb/IIIa interactions, and PI3-K in adrenaline's procoagulant response, suggesting that targeting these pathways and increasing cAMP could effectively manage PS exposure in platelets.
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Purinergic signaling, the oldest evolutionary transmitter system, has been increasingly studied as a pivotal target for novel anti-cancer therapies. In the present work, the developed nanobiocatalytic system consisting of adenylate kinase immobilized on graphene oxide (AK-GO) was characterized in terms of its physicochemical and biochemical properties. We put special emphasis on the AK-GO influence on purinergic signaling components, that is, ecto-nucleotides concentration and ecto-enzymes expression and activity in human lung carcinoma epithelial (A549) cells.

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To design new material for blood-related applications one needs to consider various factors such as cytotoxicity, platelet adhesion, or anti-thrombogenic properties. The aim of this work is the design of new, highly effective materials possessing high blood compatibility. To do this, the new composites based on the poly(vinylidene fluoride) (PVDF) support covered with a single-walled carbon nanohorns (CNHs) layer were prepared.

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  • Activated neutrophils produce myeloperoxidase (MPO), which generates hypochlorous acid (HOCl) that can disrupt blood clotting by inhibiting platelet aggregation and increasing fibrin density.
  • The study examined the effects of three antioxidant plant-derived polyphenols: quercetin (Que), epigallocatechin gallate (EGCG), and resveratrol (Resv) on the hemostatic disturbances caused by HOCl.
  • Que and EGCG were found to reverse the negative effects of HOCl on platelet aggregation and fibrin density, whereas Resv increased HOCl's inhibitory effects, suggesting that Que and EGCG could help normalize blood coagulation
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