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Consequently, recent systematic reviews have concluded that although scarce available evidence suggests that FGF-2 significantly improves defect fill but it does not have an effect on clinical attachment level gain [ 56].
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This work aims at improving defect tolerance in FPGAs which are certainly affected by technology downsizing.
Specifically, they reported significantly improved defect filling, border repair integration and surface tissue repair along with far less evidence of fissuring and fibrillation in OLTs treated with BMAC (Hannon et al. 2016).
We now plan to use principles of functional tissue engineering to determine if repairs containing central regions of longer MSC-collagen constructs improve defect repair biomechanics after implantation at surgery.
The treatment of PLLA incorporated with bFGF improved defect filling compared with that left untreated, while the regenerated tissue was mainly fibrocartilage and showed little bone formation with only a small amount of collagen type II (Col II) and no aggrecan gene message measured.
Histomorphometry revealed significantly improved defect repair in the osteoporotic ABM/P-15 group compared with the empty group.
In particular, optimizing surface chemistry, improving defect yield, and simultaneously reducing the size and preventing aggregation are still issues.
In addition, statins improved defect regeneration when locally applied in cranial/mandibular bone defect models without metal implants [ 15- 17, 36].
Although these cell-free approaches reproducibly led to good healing efficiency, combinations of ASC and recombinant BMP-2 were also used (Refs 137, 138, 139, 140, 141, 142) (not listed in Table 4), but only Levi et al. described that ASC improved defect repair in comparison to the BMP-loaded scaffold alone (Ref. 142).
It shows that the I D/I G ratio of pristine CNT is 0.721 and it increases to 0.847 after the preparation process, indicating decreased crystallinity and improved defects in the CNTs.
OPA1 can even partially improve defects caused by complete lack of mitochondrial CI via an unknown mechanism.
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