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Osteoclasts in bone form a sealing zone, which is roughly equivalent to the podosome belt.
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Since it is known that bone turnover in basic multicellular units (BMUs) is at equilibrium, inducing an imbalance in this process via molecules known to resorb and transmit resorption signals and therefore initiate activation in bone forming cells from adjacent tissue may offer a radical approach to bone regeneration.
We report an increased osteoclastogenesis in CaP bone metastatic patients, due to an increase in the serum RANKL/OPG ratio, suggesting that enhanced OC formation plays an active role in bone forming metastases.
To determine whether the structural changes in bone and the low bone formation rate observed in Lmna−/− mice are associated with a deficit in bone forming osteoblasts, analysis of osteoblastic differentiation of pluripotent bone marrow cells and osteoblast number and activity in bone tissue were performed.
Interestingly, the collagen cross-link ratio in bone forming areas had the same profile as seen in actively bone forming trabecular surfaces in human iliac crest biopsies of osteoporotic patients.
An interesting observation is the difference in bone formed on the outer threaded surface and on the inner non-threaded surface, where there was a distinct difference in the type of bone that had formed.
By 30 days after surgery, the differences in bone formed between controls and A-79175 treated defects were not significant, although the A-79175 treated defects had consistently higher BV/TV values.
We therefore speculate that Fra-1 functions in bone forming osteoblasts, mainly by affecting the activity of the cells through the regulation of matrix production and not by affecting the proliferation or differentiation of cells.
They can occur in bones formed by endochondral ossification.
In conclusion, this study demonstrates that Pcsk5 is expressed in bone-forming cells, and that OPN is a novel substrate for PC5/6.
Phex-deficient Hyp mice have been extensively studied to understand the molecular bases of XLHR, and here it was found that Fgf23, encoding a major phosphaturic hormone, was transcriptionally activated in bone-forming osteoblasts.
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