Results 41 to 50 of about 5,026,038 (351)

MIF contributes to Trypanosoma brucei associated immunopathogenicity development [PDF]

open access: yes, 2014
African trypanosomiasis is a chronic debilitating disease affecting the health and economic well-being of many people in developing countries. The pathogenicity associated with this disease involves a persistent inflammatory response, whereby M1-type ...
Beschin, Alain   +11 more
core   +4 more sources

Inflammatory Cytokines and Mucosal Injury [PDF]

open access: yesJNCI Monographs, 2001
The cause of mucosal injury in inflammatory bowel disease (IBD) is not clear but likely involves infectious agents or other toxins followed by an abnormal immune response in genetically susceptible individuals. The inflammatory cytokines appear to play a key role in both the susceptibility of some individuals and the tissue damage that accompanies IBD.
openaire   +2 more sources

Alveolar macrophages and Toll-like receptor 4 mediate ventilated lung ischemia reperfusion injury in mice. [PDF]

open access: yes, 2012
BackgroundIschemia-reperfusion (I-R) injury is a sterile inflammatory process that is commonly associated with diverse clinical situations such as hemorrhage followed by resuscitation, transient embolic events, and organ transplantation.
Dodd-o, Jeffrey M   +5 more
core   +1 more source

Antimicrobial peptides and complement in neonatal hypoxia-ischemia induced brain damage [PDF]

open access: yes, 2015
Hypoxic-ischemic encephalopathy (HIE) is a clinical condition in the neonate, resulting from oxygen deprivation around the time of birth. HIE affects 1-5/1000 live births worldwide and is associated with the development of neurological deficits ...
Hristova, M, Rocha-Ferreira, E
core   +1 more source

MiR‐22 restrains proliferation of rheumatoid arthritis by targeting IL6R and may be concerned with the suppression of NF‐κB pathway

open access: yesKaohsiung Journal of Medical Sciences, 2020
It has demonstrated that miR‐22 overexpression can suppress the inflammation process of rheumatoid arthritis (RA) in synoviocytes. But, the underlying mechanism of miR‐22 expression in regulating RA is still not well illustrated.
Qing‐Yi Yang   +2 more
doaj   +1 more source

COX2 Enhances Neovascularization of Inflammatory Tenocytes Through the HIF-1α/VEGFA/PDGFB Pathway

open access: yesFrontiers in Cell and Developmental Biology, 2021
Tendon injuries are among the most challenging in orthopedics. During the early tendon repair, new blood vessel formation is necessary. However, excessive angiogenesis also exacerbates scar formation, leading to pain and dysfunction.
Bin Deng   +4 more
doaj   +1 more source

Nlrp6 promotes recovery after peripheral nerve injury independently of inflammasomes [PDF]

open access: yes, 2015
Background: NOD-like receptors (Nlrs) are key regulators of immune responses during infection and autoimmunity. A subset of Nlrs assembles inflammasomes, molecular platforms that are activated in response to endogenous danger and microbial ligands and ...
De Winter, Vicky   +6 more
core   +2 more sources

Inhibition of inflammatory liver injury by the HMGB1-A box through HMGB1/TLR-4/NF-κB signaling in an acute liver failure mouse model

open access: yesFrontiers in Pharmacology, 2022
We aimed to investigate the preventive effect of high mobility group box 1 (HMGB1)-A box and the mechanism by which it alleviates inflammatory injury in acute liver failure (ALF) by inhibiting the extracellular release of HMGB1.
Lidan Luo   +11 more
doaj   +1 more source

Inflammation-induced DNA damage and damage-induced inflammation: a vicious cycle [PDF]

open access: yes, 2014
Inflammation is the ultimate response to the constant challenges of the immune system by microbes, irritants or injury. The inflammatory cascade initiates with the recognition of microorganism-derived pathogen associated molecular patterns (PAMPs) and ...
Abe   +100 more
core   +1 more source

Trimethylamine-N-Oxide Aggravates Kidney Injury via Activation of p38/MAPK Signaling and Upregulation of HuR

open access: yesKidney & Blood Pressure Research, 2021
Background: Trimethylamine-N-oxide (TMAO) is an intestinal metabolic toxin, which is produced by gut flora via metabolizing high-choline foods. TMAO is known to increase the risk of atherosclerosis and cardiovascular events in chronic kidney disease (CKD)
Yunshi Lai   +8 more
doaj   +1 more source

Home - About - Disclaimer - Privacy