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Transfusion in trauma: empiric or guided therapy?
Res Pract Thromb Haemost
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Oxford Haemophilia and Thrombosis Centre, Department of Haematology, Oxford University Hospitals National Health Service Foundation Trust, Nuffield Orthopaedic Centre, Oxford, UK.
A state of the art lecture titled "Transfusion therapy in trauma-what to give? Empiric vs guided" was presented at the International Society on Thrombosis and Haemostasis Congress in 2024. Uncontrolled bleeding is the commonest preventable cause of death after traumatic injury. Hemostatic resuscitation is the foundation of contemporary transfusion practice for traumatic bleeding and has 2 main aims: to immediately support the circulating blood volume and to treat/prevent the associated trauma-induced coagulopathy.
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Department of Biochemistry and Biotechnology, University of Thessaly, Viopolis, Mezourlo, Larissa 41500, Greece.
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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with a complex etiology primarily linked to abnormalities in B lymphocytes within the human body, resulting in the production of numerous pathogenic autoantibodies. Telitacicept is a relatively novel humanized, recombinant transmembrane activator, calcium modulator and cyclophilin ligand interactor fused with the Fc portion (TACI-Fc). It works by competitively inhibiting the TACI site, neutralizing the activity of B-cell lymphocyte stimulator and A proliferation-inducing ligand.
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Neuroscience Center, HiLIFE, University of Helsinki, Helsinki, Finland.
Introduction: The neuron-specific K-Cl cotransporter KCC2 maintains low intracellular chloride levels, which are crucial for fast GABAergic and glycinergic neurotransmission. KCC2 also plays a pivotal role in the development of excitatory glutamatergic neurotransmission by promoting dendritic spine maturation. The cytoplasmic C-terminal domain (KCC2-CTD) plays a critical regulatory role in the molecular mechanisms controlling the cotransporter activity through dimerization, phosphorylation, and protein interaction.
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Vitiligo is a common skin depigmentation condition caused by selective destruction of melanocytes. It is regarded as a polygenic disorder. In addition to protein-coding loci, non-coding regions of the genome contribute to the pathogenesis of vitiligo.
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