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Expression level of cartilage marker genes was elevated in all cultures showing that dedifferentiation of chondrocytes could be prevented.
The level of cartilage associated ECM proteins was examined by immunohistochemical staining (collagen types II and X) as well as by Safranin-O and Alcian blue (GAG) staining.
The level of cartilage degradation was assessed by measurement of CTXII levels.
This elevation is an indication of an increased level of cartilage degradation.
The expression level of cartilage- and tendon-expressed genes [ 1] also returned to baseline levels following overuse/rest protocol.
The glucosamine treatment group showed a lower level of cartilage degradation and synovial inflammation compared to the control group.
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The level of cartilage-related transcripts (AGC, Col-II, Sox 9 and Col-II/Col-I ratio) and the deposition of cartilage-specific ECM were significantly upregulated in constructs initiated with higher seeding density.
Both the differentiation and level of cartilage-specific ECM production were significantly higher in the presence of HA and growth factor than in the control without the growth factor.
In an attempt to determine how DR-3 so rapidly contributes to joint degradation, we investigated the level of cartilage-destroying enzymes within the joints of DR3−/− and WT mice in early AIA.
To compare the MANKIN and OARSI cartilage histopathology assessment systems using human articular cartilage from a large number of donors across the adult age spectrum representing all levels of cartilage degradation.
Correspondingly, chondrocytes cultured in silk and collagen scaffolds maintained higher levels of cartilage matrix than those in PLA, suggesting that these biophysical properties of scaffolds may regulate gene expression and the response to inflammatory stimuli in chondrocytes.
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