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In vivo animal bone-defect experiments showed dose-dependent bone formation using the PTH fibrin matrix, with evidence of both osteoconductive and osteoinductive bone-healing mechanisms.
Because of the reduced potential for bone growth in patients over the age of 25 [13], there might be some impaired bone formation using the callotasis lengthening technique in elderly patients.
We then tested the efficacy of both 25 μM and 50 μM on bone formation using the Matrigel/rhBMP ectopic ossification CD-1 mouse strain model.
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Liu et al. observed the bone formation using beagle deep fascia pedicled flap wrapping the tissue engineered bone and they found that the new blood vessels of tissue engineered bone in the fascia flap group were superior to those in the control group, suggesting that pedicled fascia flap could promote the revascularization of tissue engineered bone in vivo [ 31].
These BMP-2 induced bone quantities come into the range of the new bone formation using PCL noncoated or PCL coll I/cs coated scaffolds without any growth factor application, indicating that the PCL scaffold by itself acts beyond osteoconductive properties.
The aim of this study was to evaluate the ectopic bone formation using tissue engineered cell-seeded constructs with two different scaffolds and primary human maxillary osteoblasts in nude rats over an implantation period of up to 96 days.
Sun et al. (2009) analyzed the effect of BMC on vascularisation and bone formation using a steroid-induced osteonecrosis model of the femoral head in rabbits.
Two independent investigators masked to the groups of cells estimated the degree of bone formation using a semi-quantitative scale as previously described [23].
It has been speculated that the reduced bone formation using local treatment is caused by unbound bisphosphonate being released, reaching high tissue concentrations also in vivo.
Arguing the importance of load-transduction, we investigated the mechanisms inducing bone formation using an elastomeric substrate.
We also sought to investigate the molecular changes underlying the progression through inflammation to bone formation using whole-genome expression analysis.
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