Results 171 to 180 of about 4,621,354 (401)

Surprising lack of liposome-induced complement activation by artificial 1,3-diamidophospholipids in vitro [PDF]

open access: yes, 2016
Cardio-vascular diseases are the main cause of death, emphasizing the need to improve patient treatment and survival. One therapeutic approach is a liposome-based drug carrier system specifically targeting constricted arteries. The recently discovered
Barratt   +15 more
core   +1 more source

Evaluation of KRAS and NRAS mutations in metastatic colorectal cancer: an 8‐year study of 10 754 patients in Turkey

open access: yesMolecular Oncology, EarlyView.
This nationwide study evaluated KRAS and NRAS mutations in 10 754 Turkish patients with metastatic colorectal cancer. The results revealed a mutation frequency of 51.1%, with 46.6% having KRAS mutations, 4.5% having NRAS mutations, and 48.5% being wild‐type for both.
Gozde Kavgaci   +6 more
wiley   +1 more source

Persistent Intracellular Staphylococcus aureus in Keratinocytes Lead to Activation of the Complement System with Subsequent Reduction in the Intracellular Bacterial Load

open access: yesFrontiers in Immunology, 2018
The complement system is an ancient part of the innate immune system important for both tissue homeostasis and host defense. However, bacteria like Staphylococcus aureus (SA) possess elaborative mechanisms for evading both the complement system and other
Anas H. Abu-Humaidan   +5 more
doaj   +1 more source

C1q-targeted inhibition of the classical complement pathway prevents injury in a novel mouse model of acute motor axonal neuropathy [PDF]

open access: yes, 2016
Introduction Guillain-Barré syndrome (GBS) is an autoimmune disease that results in acute paralysis through inflammatory attack on peripheral nerves, and currently has limited, non-specific treatment options.
Barrie, Jennifer A.   +8 more
core   +2 more sources

Eculizumab reduces complement activation, inflammation, endothelial damage, thrombosis, and renal injury markers in aHUS.

open access: yesBlood, 2015
Atypical hemolytic uremic syndrome (aHUS) is a genetic, life-threatening disease characterized by uncontrolled complement activation, systemic thrombotic microangiopathy (TMA), and vital organ damage.
R. Cofiell   +7 more
semanticscholar   +1 more source

Loss of proton‐sensing GPR4 reduces tumor progression in mouse models of colon cancer

open access: yesMolecular Oncology, EarlyView.
G protein‐coupled receptor 4 (GPR4) is a pH‐sensing receptor activated by acidic pH. GPR4 expression is increased in patients with inflammatory bowel disease who are at high risk of developing colorectal cancer. In mouse models, loss of GPR4 attenuated tumor progression. This correlated with increased IL2 and natural killer cell activity.
Leonie Perren   +16 more
wiley   +1 more source

Material properties in complement activation

open access: yesAdvanced Drug Delivery Reviews, 2011
Uncontrolled complement activation can induce many inflammatory and life threatening conditions. Accordingly, the role of complement in initiation of adverse reactions to polymers and nanoparticulate drug carriers is receiving increasing attention and has prompted extensive 'structure-immune performance' relationship studies in nanomedicine research at
Moghimi, Seyed Moein   +5 more
openaire   +5 more sources

Dose‐dependent induction of epithelial‐mesenchymal transition in 3D melanoma models by non‐thermal plasma treatment

open access: yesMolecular Oncology, EarlyView.
Non‐thermal plasma treatment of melanoma cells induced epithelial‐mesenchymal transition (EMT) in a dose‐dependent fashion. This report highlights the critical need to further investigate potential adverse effects of non‐thermal plasma for cancer therapy and to optimize treatment parameters for clinical translation. Despite the promising results of non‐
Eline Biscop   +10 more
wiley   +1 more source

The Tutte q-Polynomial [PDF]

open access: yesarXiv, 2017
$q$-Matroids are defined on complemented modular support lattices. Minors of length 2 are of four types as in a "classical" matroid. Tutte polynomials $\tau(x,y)$ of matroids are calculated either by recursion over deletion/contraction of single elements, by an enumeration of bases with respect to internal/external activities, or by substitution $x \to
arxiv  

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