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Nano-sized and micro-sized ZnWO4 powders were obtained by different methods: hydrothermal synthesis with microwave heating, molten salt method, solid-state synthesis and сrushing of bulk crystals. Their morphological features were studied using transmission electron microscope and scanning electron microscope. The obtained nano- and micro-sized powders were used as fillers for flexible composite scintillators. The silicon rubber was used as a binder. The luminescent characteristics and scintillation performance of composite scintillators were measured. The dependence of scintillation performance of flexible scintillators on the morphological features of ZnWO4 nanocrystallites was demonstrated. The flexible composite scintillator based on zinc tungstate obtained by solid-state synthesis with lithium nitrate addition was obtained and investigated. Its scintillation performance was close to that of a ZnWO4 single crystal.

Background: Free labile hemin acts as a damage-associated molecular pattern during acute and chronic hemolysis and muscle injury, supporting platelet activation and thrombosis., Objectives: To investigate the anti-thrombotic potential of hydroxychloroquine on hemolysis-induced platelet activation and arterial thrombosis., Methods: The effect of hydroxychloroquine on hemin-induced platelet activation and hemolysis-induced platelet recruitment and aggregation was measured in washed platelets and hemolyzed blood, respectively. Its effect on ferric-chloride (FeCl 3 )-induced arterial thrombosis and lung perfusion following hemin injection was assessed in wild-type mice., Results: Erythrocyte lysis and endothelial cell activation cooperatively supported platelet aggregation and thrombosis at arterial shear stress. This thrombotic effect was reversed by hydroxychloroquine. In a purified system, hydroxychloroquine inhibited platelet build-up on immobilized von Willebrand factor in hemolyzed blood without altering initial platelet recruitment. Hydroxychloroquine inhibited hemin-induced platelet activation and phosphatidylserine exposure independently of reactive oxygen species generation. In the presence of hemin, hydroxychloroquine did not alter glycoprotein VI shedding but reduced C-type-lectin-like-2 expression on platelets. In vivo, hydroxychloroquine reversed pulmonary perfusion decline induced by exogenous administration of hemin. In arterial thrombosis models, hydroxychloroquine inhibited ferric-chloride-induced thrombosis in the carotid artery and reduced von Willebrand factor accumulation in the thrombi., Conclusion: Hydroxychloroquine inhibited hemolysis-induced arterial thrombosis ex vivo and improved pulmonary perfusion in hemin-treated mice, supporting a potential benefit of its use as an adjuvant therapy in hemolytic diseases to limit arterial thrombosis and to improve organ perfusion., Competing Interests: Declaration of competing interests There are no competing interests to disclose., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)