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Burkhart and De Beer [9] suggested defect orientation was more important, differentiating "engaging" from "non-engaging" Hill Sachs lesions.
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Early studies suggested defects in the mitotic checkpoint as the main cause of CIN [7].
The morphology observed in lung epithelial cells after LT exposure suggested defects in cell functions, which rely on directed migration such as chemotaxis or wound healing.
It displayed developmental phenotypes that suggested defects in auxin transport or responsiveness.
Our previous analysis suggested defects in ALPM formation in aplnrb morphants (morpholino-injected embryos) and mutants (Scott et al., 2007).
MPE animal models and immunotherapy trials in MPM patients previously suggested defects of the cellular immunity in MPE.
The blunted blood vessel morphologies at P5 and tufted vascular structures at P14 suggested defects in endothelial cell proliferation and/or sprouting in β8 /– retinas.
In addition there was variability in shape of the signal in AtCTF7-RNAi plants compared to untreated control plants which suggested defects in centromere organization.
Most anecdotal evidence suggests defects larger than 20%% of the humeral head require surgical management.
The microtubule location suggests defects in the cell wall and repair which were also suggested for actin [36].
Moreover, there was abnormal "pitting" in the ommatidia, suggesting defects in the cone cells that secrete the lens material [22; Figure 3G, arrow].
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CEO of Professional Science Editing for Scientists @ prosciediting.com