Various characterization techniques, namely, transmission electron microscopy (TEM), low temperature μ-photoluminescence (PL), Raman spectroscopy and current (I -voltage I -voltageements were used to ascertain the nature of defects being annihilated.
These tests ascertain the type of defect, for example, obstructive or restrictive ventilatory defects, which helps establish the cause, such as an exacerbation of any underlying obstructive airways disease versus interstitial disease.
Further work is clearly to ascertain the origin of these defects.
From our data we cannot ascertain whether the defect observed for the L2 cysteine mutants comes from the lack of the C22 C28 disulfide structure or whether it is a consequence of a failed interaction/binding between the exposed RG-1 epitope and an unknown host receptor due to the replacement of cysteines with serines.
Attention must be paid to individual ocular as well as facial characteristics when interpreting visual fields, in order to ascertain the likely cause of any individual field defect.
We examined 1A-/ 1B-/ double mutant seedling roots via bright field microscopy to ascertain the extent of their post-embryonic growth defect.
rpoC* and rrn deletion alleles (Δ rrnE and Δ rrnB, Supplementary Figure S1) were used to ascertain the role of rrn in the observed growth defects.
Detailed understanding of the atomic arrangement along the GB, in addition to defect density, is necessary to ascertain the ultimate strength and rupture process of GBs.
To further ascertain the cellular changes occurring in GD18 LPS-exposed foetal forebrains that might underlie the defect in neuronal patterning, we examined the expression levels and distribution of GLAST, a marker for radial glia.
We sought to ascertain the risk of reduced fetal brain growth in cases of isolated congenital heart defect (CHD) based on microcephaly at birth.
