Results 101 to 110 of about 20,066 (195)

Targeting complement C5a to improve radiotherapy sensitivity in non-small cell lung cancer. [PDF]

open access: yesTransl Lung Cancer Res, 2023
Yuan M   +18 more
europepmc   +1 more source

Neutrophils from ANCA-associated vasculitis patients show an increased capacity to activate the complement system via the alternative pathway after ANCA stimulation.

open access: yesPLoS ONE, 2019
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides (AAV), including granulomatosis with polyangiitis (GPA) and microscopic polyangiitis (MPA), are autoimmune conditions associated with small vessel inflammation.
Sophie Ohlsson   +6 more
doaj   +1 more source

Projecting future damage costs of non‐native species using combined dynamical and cost–density equations

open access: yesEcological Applications, Volume 36, Issue 5, July 2026.
Abstract Biological invasions threaten biodiversity, economic stability, and public health, exacerbated by intensive global trade and transport. The economic costs of these invasions have exceeded US$2 trillion globally and continue to increase. Although past invasion costs have been described across various contexts, there are few robust projections ...
Danish A. Ahmed   +11 more
wiley   +1 more source

Complement Inhibition in the Clinic: Are We Doing Enough to Protect Patients From Infection?

open access: yesEuropean Journal of Immunology, Volume 56, Issue 7, July 2026.
Excessive complement activation is implicated in a broad range of diseases. Therapeutic approaches targeting the complement cascade, from pathway‐selective inhibition to terminal blockade, can effectively control disease activity. However, increasing degrees of complement inhibition are associated with a heightened susceptibility to bacterial, viral ...
Serena Bettoni   +4 more
wiley   +1 more source

Reduced Complement and Granulocyte Activation by α‐Gal Knockout Porcine Pericardium for Bioprosthetic Heart Valves: A Pilot Hemocompatibility Study

open access: yesJournal of Biomedical Materials Research Part A, Volume 114, Issue 7, July 2026.
Genetically modified, α‐Gal‐depleted porcine pericardium and wild type tissues are investigated for hemocompatibility and material properties such as mechanobiology and ECM profile to carve out the suitability of the gene‐modified tissue as material for biological heart valve prostheses. ABSTRACT Xenogeneic pericardium is the main source for biological
Claudia Dittfeld   +7 more
wiley   +1 more source

Ischemia–Reperfusion Injury: Molecular Mechanisms and Therapeutic Interventions

open access: yesMedComm, Volume 7, Issue 7, July 2026.
Multiorgan ischemia–reperfusion injury begins with ischemia‐induced ATP depletion and ionic imbalance, followed by reperfusion‐triggered mitochondrial ROS/RNS bursts, regulated cell death, and DAMP release. Sterile inflammation converges on endothelial–immune–coagulation crosstalk, where NETs drive immunothrombosis, no‐reflow, and remote organ injury ...
Peng An   +4 more
wiley   +1 more source

C3a and C5a plasma concentrations in patients with diabetic retinopathy: a cross-sectional study

open access: yesInternational Journal of Retina and Vitreous
Background Diabetic retinopathy (DR) is the leading cause of irreversible blindness in adults, with inflammation playing a critical role in its pathogenesis, particularly involving the complement system (CS). Components of the complement cascade, such as
Paula Basso Dias   +4 more
doaj   +1 more source

Evidence for a Two‐Step Model for Activation of GPR25 by the Chemoattractant CXCL17

open access: yesBasic &Clinical Pharmacology &Toxicology, Volume 139, Issue 1, July 2026.
ABSTRACT CXCL17 was recently reported to activate GPR25, a receptor expressed by T‐regulatory cells. Although classified as a chemokine, the activity of CXCL17 is ablated by minor C‐terminal truncation, suggesting a novel mode of receptor activation. We set out to test this hypothesis by mutagenesis. GPR25 was expressed in the murine pre‐B cell line L1.
Wuqing Yang   +2 more
wiley   +1 more source

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