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Vascular injuries and hemorrhaging are serious potential complications in the management of patients with blunt abdominal trauma. The treatment depends on the extent and localization and can range from surveillance to endovascular treatment up to open surgery. The keys to success include the focused assessment with sonography for trauma (FAST) management and timely decision making. Abdominal vascular trauma continues to be a difficult problem and open and endovascular techniques continue to evolve in order to address this complex disease process., (© 2023. The Author(s).)

Background: The research consortium Neuroimmunology and Pain (Neuroimpa) explores the importance of the relationships between the immune system and the nervous system in musculoskeletal diseases for the generation of pain and for the course of fracture healing and arthritis., Material and Methods: The spectrum of methods includes analyses at the single cell level, in vivo models of arthritis and fracture healing, imaging studies on brain function in animals and humans and analysis of data from patients., Results: Proinflammatory cytokines significantly contribute to the generation of joint pain through neuronal cytokine receptors. Immune cells release opioid peptides which activate opioid receptors at peripheral nociceptors and thereby evoke hypoalgesia. The formation of new bone after fractures is significantly supported by the nervous system. The sympathetic nervous system promotes the development of immune-mediated arthritis. The studies show a significant analgesic potential of the neutralization of proinflammatory cytokines and of opioids which selectively inhibit peripheral neurons. Furthermore, they show that the modulation of neuronal mechanisms can beneficially influence the course of musculoskeletal diseases., Discussion: Interventions in the interactions between the immune system and the nervous system hold a great therapeutic potential for the treatment of musculoskeletal diseases and pain.

The Research Consortium IMPAM (IMprinting of the PAthogenic Memory for rheumatic inflammation) has recently been funded by the Federal Ministry of Education and Research in Germany. Within this consortium ten different research groups, coordinated by the German Rheumatism Research Center (DRFZ) and the University Hospital Jena, will examine the molecular dialogue between immune system memory cells and mesenchymal cells in chronic rheumatic diseases, such as rheumatoid arthritis or ankylosing spondylitis. The consortium's aim is to understand and modulate these interactions therapeutically, such that the pathogenic imprinting of proinflammatory memory cells can be extinguished and the anti-inflammatory capacity of the patients' regulatory cells can be restored.

The intestinal microbiota contributes to the regulation of the intestinal immune system and protection against intestinal infections. Recent studies revealed that the locally restricted intestinal microbiota affects systemic immunity and influences the induction of autoimmunity.

State-of-the-art immunosuppressive therapies, though efficient in the treatment of rheumatic inflammatory disorders, in most cases do not provide a cure. Complete immunablation and the associated deletion of the reactive immunological memory followed by reconstitution of the "healthy" immune system from stem cells results in a therapy-free remission in many patients suffering from rheumatic diseases. Chronically activated T helper (Th) lymphocytes seem to play a critical role in this reactive pathogenic memory. We have shown that the transcription factor twist1 is specifically expressed in chronically activated, inflammatory Th cells. Twist1 as a biomarker for such Th cells enables the identification and elucidation of the role of Th cells in chronic inflammation and opens new therapeutic options for the targeted manipulation of the pathogenic, reactive memory, such as the targeted deletion of twist1 expressing pathogenic Th cells.