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The previous component, cement, and membrane were removed and the acetabular defect was confirmed intraoperatively.
After the first evidence by Schoenen et al in 1995[1] of reduced habituation to visual evoked potentials in migraine the defect was confirmed in other studies, not only with visual stimuli, but also with other sensory modalities (acoustic, somatosensory) and even with nociceptive stimulation.
In the remaining cases, the pregnancy course was terminated and the defect was confirmed in elected autopsies.
This cell-fate defect was confirmed by another PFC fate marker, 667/9-lacZ (Gonzalez-Reyes, Elliot, Deng, Pathirana, Deak, Glover, St Johston, and Bownes, unpublished data) (Fig. 2D).
This suspected defect was confirmed and quantified by analyzing permeabilized and nonpermeabilized cells by flow cytometry after various treatments.
This defect was confirmed in co-culture experiments using a mixture of control and p66Shc-expressing MEC cells labeled with different fluorescent probes.
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The incorporation of nitrogen (N) atoms and defects are confirmed by X-ray photoelectron spectroscopy and Raman spectroscopy.
The regeneration defects were confirmed by staining Fir1 RNAi) trunk pieces with gastrointestinal system marker (Porcupine) and nervous system marker (PC2) 8 days post-amputation (Fig. 2B).
Clinical improvements were achieved at 6 months post-surgery, and at 12 months post-surgery the defects were confirmed to be filled while one of the cases' histology indicated a fibrocartilaginous tissue in the defect, not hyaline cartilage (Wakitani et al. 2007).
The previously reported phenotypic overlaps with VACTERL, caudal dysgenesis, hemifacial microsomia and Müllerian defects were confirmed.
In cases resulting in live newborns, the defects were confirmed postnatally.
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