Feprazone Ameliorates TNF-α-Induced Loss of Aggrecan via Inhibition of the SOX-4/ADAMTS-5 Signaling Pathway. [PDF]
Xiong X +6 more
europepmc +1 more source
The design of a randomized, placebo-controlled, dose-ranging trial to investigate the efficacy and safety of the ADAMTS-5 inhibitor S201086/GLPG1972 in knee osteoarthritis. [PDF]
Imbert O +9 more
europepmc +1 more source
A CASE OF THROMBOTIC THROMBOCYTOPENIC PURPURA RELATED TO MALIGNITY AND CHEMOTHERAPY
Objective: Thrombotic thrombocytopenic purpura (TTP) is a life-threatening multisystem disease. TTP progresses with Microangiopathic hemolytic anemia (MAHA), fever, thrombocytopenia, neurological symptoms, and renal failure.
Ebru Kavak Yavuz +5 more
doaj +1 more source
Bisphosphonates (BP) are considered a treatment option for osteoarthritis (OA) due to reduction of OA-induced microtrauma in the bone marrow, stabilization of subchondral bone (SB) layer and pain reduction.
Marianne Ehrnsperger +4 more
doaj +1 more source
The Anti-ADAMTS-5 Nanobody® M6495 Protects Cartilage Degradation Ex Vivo. [PDF]
Siebuhr AS +8 more
europepmc +1 more source
Background Thrombotic thrombocytopenic purpura (TTP) is an uncommon and life-threatening disorder caused by a deficiency of ADAMTS-13, and eventually leads to microangiopathic hemolytic anemia, severe thrombocytopenia, and organ damages. Acute TTP events
Geng-Hao Bai +4 more
doaj +1 more source
In vitro characterization of the ADAMTS-5 specific nanobody® M6495 [PDF]
D. Werkmann +9 more
openaire +1 more source
Early mRNA expression of pro-inflammatory cytokines and ADAMTS-5 in an acute ischemia/reperfusion-induced pressure ulcer model, a pilot exploratory animal study. [PDF]
Sağlam M +6 more
europepmc +1 more source
Mitochondrial dysfunction activates ADAMTS-5 expression via mt-dsRNA-PKR-Spi-1 axis in osteoarthritic chondrocytes. [PDF]
Mu Y +8 more
europepmc +1 more source
P129 | Diagnostic pathway for thrombotic thrombocytopenic purpura: Case study
Premises: TTP is characterized by MAHA with thrombocytopenia and organ ischemia. The diagnosis is confirmed by a severe deficiency in ADAMTS 13 activity, either congenital or immune-mediated.
doaj +1 more source

