We sought a sample with optimal opportunities for fetal growth for the creation of standard both because this is the logical standard and also to avoid the problem of the varying incidence of growth restricting pathology and environmental exposures between populations.
Our results indicate that the proportional deviation of OWBW from OWUS was statistically significant prior to 28 weeks gestation, after accounting for individualised growth potential and excluding those with diagnosed growth restriction or known growth restricting pathologies.
However, their inclusion of individuals subsequently born pre-term, those exposed to maternal smoking during pregnancy, and those with known growth restricting pathologies would have deflated the true discrepancy.
The observed variation in intra-uterine growth rates between ethnic groups [ 7, 6] may reflect genetically determined differences in optimal rates and/or systematic differences in incidence of growth restricting pathologies and/or environmental exposures.
For example, in Western Australian (WA) Indigenous communities the tendency to slower fetal growth relative to Caucasians is believed to be primarily a result of a higher incidence of growth restricting pathologies and environmental exposures [ 11].
The proportion of optimal equivalences in Table 7 will over-estimate the appropriateness of growth of percentile defined groups to an extent depending on the burden of growth restricting pathologies in their reference sample.
For example, a newborn with a POBW of 85% might be at the 20th percentile position of the birth weight distribution for a population with a high burden of growth restricting pathologies, but the 8th percentile of a population with optimal fetal growth.
In the period to which this study was restricted (1990 to 2001), pathology laboratories in general routinely performed ER/PR testing of breast cancer.
The effect of ChABC on diffuse pathology is not restricted to tau pathology, because in a recent experiment ChABC was injected into the hippocampus of transgenic mice with an amyloidopathy model of neurodegenerative disease (APP/PSI mice), demonstrating restoration of fear memory and in increase in LTP (Vegh et al., 2014).
In this study, none of the oldest old patients with dementia and brainstem restricted Lewy body pathology met the pathological criteria for AD, suggesting that an additional pathological process may have been responsible for their dementia [ 47].
