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In this case the results of Jain et al. [ 19] may be explained by the origin of osteosarcomas in their model in bone progenitor cells, which we assume were able to avoid c-Myc-induced apoptosis.
In Ewing's sarcoma, ZA has been shown to inhibit proliferation on ES cell lines in vitro and to slow the tumor growth in a mouse ES model in bone [ 18].
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Our previous studies showed a strong therapeutic potential of ZA as it inhibits ES cell growth in vitro and ES primary tumor growth in vivo in a mouse model developed in bone site.
By using a loading regimen that stimulated woven bone formation, we sought to provide a stringent test for the presence of regional or systemic influences on mechanically adaptive (re)modelling in bones other than those being loaded.
The narrow implication of these findings is that since loading of one bone at physiological levels does not influence (re)modelling in bones that are contra-lateral, adjacent or remote to the bones that are loaded, the contra-lateral bones can be used as non-loaded controls.
We present a 3D wound healing model in engineered bone tissue that serves as a pre-clinical experimental platform for studying electrophysiological regulation of wound healing.
This contrasts the ACLT model in which bone volume fraction was clearly reduced at 10 and 20 weeks (15 20%).
In contrast, a screw model in shaft bone would not yield relevant information as fixation would largely be dependent on the pre-existing cortex, and not on newly formed bone.
There is strong evidence from animal studies that Cox-2 inhibitors delay bone healing in diaphyseal fracture models (Zhang et al. 2002, Seidenberg and An 2004, Gerstenfeld et al. 2007, Saudan et al. 2007), and small effects have also been found in a stable fixation model in metaphyseal bone in rats (Meunier and Aspenberg 2006).
Several groups have developed in vivo models in which bone or bone substitutes are implanted in animals.
As for all xenograft models, metastases in bone are not observed following orthotopic injection; tumor cells are therefore injected directly into the left ventricle of the heart.
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