The phrase "absence of developmental" is correct and usable in written English.
It can be used in contexts discussing the lack of growth or progress in a particular area, such as education, psychology, or biology.
Example: "The absence of developmental milestones in the child's growth raised concerns among the pediatricians."
Alternatives: "lack of development" or "deficiency in development".
More specifically, the absence of developmental reproductive hormone exposure in hpg females restricted the AVPV kisspeptin neuronal population size and/or Kiss1 expression at puberty.
The almost identical response to thermal stress in holobionts grown out in two different environments suggests an absence of developmental plasticity for thermo-tolerance.
Subsequent work has debated whether merely 'social costs', in the absence of developmental costs, really are sufficient to guarantee honest and evolutionarily stable signaling, conveying aspects of 'quality', such as fighting or parental ability [6], [7].
In summary, the absence of developmental proteome alterations as well as a down-regulation of proteins related to plasticity suggest the disturption of a normally occurring peak of hippocampal plasticity during adolescence in APP23 mice.
These results indicate that the absolute level of Raf protein expression is not a critical parameter and that the absence of developmental phenotype in Δ8b and Δ9b knockout mice is not likely to be due to compensatory mechanisms.
Taken together, the absence of developmental proteome alterations as well as the predominant down-regulation of neuron-specific proteins in APP23 mice indicate an interference of transgenic APP with mechanisms that generate the naturally occurring peak in hippocampal plasticity during adolescence in wildtype mice.
Apparently, the large difference in the hippocampal protein patterns between two-month old APP23 and wildtype mice was caused by the absence of distinct developmental changes in the hippocampal proteome of APP23 mice.
The absence of reported developmental defects in the Mbnl2-deficient mice might be due to evolutionary divergence.
The absence of obvious developmental defects in p53 knockout mice strongly suggests that p53 is not required for development [ 11].
Evidence of relevant signaling disruption in the absence of adequate developmental toxicology data should influence the size of the uncertainty factors used in risk assessments.
Neurodevelopmental assessments at twelve months adjusted age are strongly predictive of the presence or absence of major developmental impairments persisting at least through eight years of age [ 32].
