Results 51 to 60 of about 638,552 (336)

Blood protein adsorption onto chitosan [PDF]

open access: yes, 2002
Chitosan was recently indicated to enhance osteogenesis, improve wound healing but to activate the coagulation and the complement systems. In the present study approximately 10nm thick chitosan film were prepared on aminopropyltriethoxysilane (APTES ...
Benesch, Johan, Tengvall, P.
core   +1 more source

The epithelial barrier theory proposes a comprehensive explanation for the origins of allergic and other chronic noncommunicable diseases

open access: yesFEBS Letters, EarlyView.
Exposure to common noxious agents (1), including allergens, pollutants, and micro‐nanoplastics, can cause epithelial barrier damage (2) in our body's protective linings. This may trigger an immune response to our microbiome (3). The epithelial barrier theory explains how this process can lead to chronic noncommunicable diseases (4) affecting organs ...
Can Zeyneloglu   +17 more
wiley   +1 more source

NETosing neutrophils activate complement both on their own NETs and bacteria via alternative and non-alternative pathways

open access: yesFrontiers in Immunology, 2016
Neutrophils deposit antimicrobial proteins such as myeloperoxidase and proteases on chromatin, which they release as neutrophil extracellular traps (NETs). Neutrophils also carry key components of the complement alternative pathway (AP) such as properdin
Joshua eYuen   +10 more
doaj   +1 more source

Complement C3 variant and the risk of age-related macular degeneration [PDF]

open access: yes, 2007
Background: Age-related macular degeneration is the most common cause of blindness in Western populations. Susceptibility is influenced by age and by genetic and environmental factors.
Armbrecht, AM   +16 more
core   +1 more source

Overview of Complement Activation and Regulation

open access: yesSeminars in Nephrology, 2013
Complement is an important component of the innate immune system that is crucial for defense from microbial infections and for clearance of immune complexes and injured cells. In normal conditions complement is tightly controlled by a number of fluid-phase and cell surface proteins to avoid injury to autologous tissues.
M. Noris, G. Remuzzi
openaire   +3 more sources

From omics to AI—mapping the pathogenic pathways in type 2 diabetes

open access: yesFEBS Letters, EarlyView.
Integrating multi‐omics data with AI‐based modelling (unsupervised and supervised machine learning) identify optimal patient clusters, informing AI‐driven accurate risk stratification. Digital twins simulate individual trajectories in real time, guiding precision medicine by matching patients to targeted therapies.
Siobhán O'Sullivan   +2 more
wiley   +1 more source

Cholesterol crystal-induced endothelial cell activation is complement-dependent and mediated by TNF [PDF]

open access: yes, 2016
Cholesterol crystals are known to be a hallmark of atherosclerosis with recent studies demonstrating deposition of these crystals in early fatty streak formation as well as penetrating the intima following plaque rupture.
Espevik, Terje   +3 more
core   +3 more sources

ERBIN limits epithelial cell plasticity via suppression of TGF‐β signaling

open access: yesFEBS Letters, EarlyView.
In breast and lung cancer patients, low ERBIN expression correlates with poor clinical outcomes. Here, we show that ERBIN inhibits TGF‐β‐induced epithelial‐to‐mesenchymal transition in NMuMG breast and A549 lung adenocarcinoma cell lines. ERBIN suppresses TGF‐β/SMAD signaling and reduces TGF‐β‐induced ERK phosphorylation.
Chao Li   +3 more
wiley   +1 more source

C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation [PDF]

open access: yes, 2015
Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation.
Agostinis, C   +9 more
core   +2 more sources

Complement activation in thrombotic microangiopathy [PDF]

open access: yesHämostaseologie, 2013
SummaryThe endothelium lining the vascular lumen is continuously exposed to complement from the circulation. When erroneously activated on host cells, complement may generate a deleterious effect on the vascular wall leading to endothelial injury, exposure of the subendothelial matrix and platelet activation.In this review the contribution of ...
Karpman, Diana, Tati, Ramesh
openaire   +4 more sources

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