Anästhesie bei Patient:innen mit postviralen Erkrankungen

Schmerz Nachrichten, Journal Year: 2025, Volume and Issue: unknown

Published: March 20, 2025

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Proteomic signatures of Post-Vaccination/Post-Infection Syndrome (PV/PIS): Insights into immune dysregulation and coagulopathy

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: May 5, 2025

During the global rollout of COVID-19 vaccines a subset individuals reported persistent symptoms following vaccination, with clinical presentations overlapping those Long COVID requiring individualised treatment decisions. Distinguishing between vaccine-related adverse events and post-infectious sequelae remains challenging, particularly given possibility asymptomatic or mild SARS-CoV-2 infection prior to after vaccination. To avoid this complexity, we define patient group as presenting Post-Vaccination/Post-Infection Syndrome (PV/PIS). In study, performed proteomic analysis plasma from 30 PV/PIS compared healthy controls. Using mass spectrometry, identified significant alterations in coagulation factors, acute phase proteins, immune response modulators group. Notably, elevated levels serum amyloid A1 A2, attractin, factors X XI were observed, alongside downregulation immune-regulatory proteins. These findings suggest that is characterized by dysregulation coagulopathy, signatures only partially previously proteomics on samples collected vaccination availability. Our results highlight complex interplay activation, endothelial dysfunction, pathologies PV/PIS, while also highlighting distinct differences these systems paving way for more targeted protein research conditions.

Language: Английский

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Proteomic evidence for amyloidogenic cross-seeding in fibrinaloid microclots

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: July 17, 2024

Abstract In classical amyloidoses, amyloid fibres form through the nucleation and accretion of protein monomers, with protofibrils fibrils exhibiting a cross-β motif parallel or antiparallel β-sheets oriented perpendicular to fibre direction. These can intertwine mature fibres. Similar phenomena occur in blood from individuals circulating inflammatory molecules (also those originating viruses bacteria). presence inflammagens, pathological clotting occur, that results an anomalous termed fibrinaloid microclots. Previous proteomic analyses these microclots have shown non-fibrin(ogen) proteins, suggesting more complex mechanism than simple entrapment. We provide evidence against entrapment model, noting clot pores are too large centrifugation would removed weakly bound proteins. Instead, we explore whether co-aggregation into may involve axial (multiple proteins within same fibril), lateral (single-protein contributing fibre), both types integration. Our analysis data different diseases shows no significant overlap normal plasma proteome correlation between abundance Notably, abundant like α-2-macroglobulin, fibronectin, transthyretin absent microclots, while less such as adiponectin, periostin, von Willebrand Factor well represented. Using bioinformatic tools including AmyloGram AnuPP, found entrapped exhibit high amyloidogenic tendencies, their integration elements structures. This likely contributes microclots’ resistance proteolysis. findings underscore role cross-seeding microclot formation highlight need for further investigation structural properties implications thrombotic diseases. insights foundation developing novel diagnostic therapeutic strategies targeting disorders.

Language: Английский

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Proteomic Evidence for Amyloidogenic Cross-Seeding in Fibrinaloid Microclots

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(19), P. 10809 - 10809

Published: Oct. 8, 2024

In classical amyloidoses, amyloid fibres form through the nucleation and accretion of protein monomers, with protofibrils fibrils exhibiting a cross-β motif parallel or antiparallel β-sheets oriented perpendicular to fibre direction. These can intertwine mature fibres. Similar phenomena occur in blood from individuals circulating inflammatory molecules (and also some originating viruses bacteria). Such pathological clotting result an anomalous termed fibrinaloid microclots. Previous proteomic analyses these microclots have shown presence non-fibrin(ogen) proteins, suggesting more complex mechanism than simple entrapment. We thus provide evidence against such entrapment model, noting that clot pores are too large centrifugation would removed weakly bound proteins. Instead, we explore whether co-aggregation into may involve axial (multiple proteins within same fibril), lateral (single-protein contributing fibre), both types integration. Our analysis data different diseases shows no significant quantitative overlap normal plasma proteome correlation between abundance their Notably, abundant like α-2-macroglobulin, fibronectin, transthyretin absent microclots, while less as adiponectin, periostin, von Willebrand factor well represented. Using bioinformatic tools, including AmyloGram AnuPP, found entrapped exhibit high amyloidogenic tendencies, integration elements structures. This likely contributes microclots’ resistance proteolysis. findings underscore role cross-seeding microclot formation highlight need for further investigation structural properties implications thrombotic diseases. insights foundation developing novel diagnostic therapeutic strategies targeting disorders.

Language: Английский

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The dysfunction of complement and coagulation in diseases: the implications for the therapeutic interventions

MedComm, Journal Year: 2024, Volume and Issue: 5(11)

Published: Oct. 23, 2024

Abstract The complement system, comprising over 30 proteins, is integral to the immune and coagulation system critical for vascular homeostasis. activation of systems involves an organized proteolytic cascade, overactivation these a central pathogenic mechanism in several diseases. This review describes role illness, particularly sepsis. complexities sepsis reveal significant knowledge gaps that can be compared profound abyss, highlighting urgent need further investigation exploration. It well recognized inflammatory network, coagulation, are mechanisms through which multiple factors contribute increased susceptibility infection may result disordered response during septic events patients. Given overlapping sepsis, immunomodulatory therapies currently under development beneficial patients with who have concurrent infections. Herein, we present recent findings regarding molecular relationships between pathways advancement propose potential intervention targets related crosstalk complement, aiming provide more valuable treatment

Language: Английский

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