According to the traditional neurocognitive view of ADHD, a core deficiency in cognitive control processes subserving the orchestration of thought and action with internal goals arises from neurodevelopmental anomalies in the prefrontal cortex [ 7].
While the traditional view of ADHD postulates a core deficiency in cognitive control processes, alternative dual-process models emphasize the dynamic interplay of bottom-up driven factors such as activation, arousal, alerting, motivation, reward and temporal processing with top-down cognitive control.
In addition, Gil et al. [ 39] suggested that SC requires a convergence of many neural networks and that the core deficiency in AD patients might be impaired SC, equated with the disability to maintain sequential and simultaneous "attention to life" [ 50, 51].
These issues are linked together by a set of core deficiencies that Obama is addressing with Race to the Top, an expanded GI Bill, and capped federal loan repayments.
The objectives for the curriculum, as found in the core syllabus, had deficiencies with respect to format, organization and specific/measurable content.
In addition, conventional adult mice with inducible deficiency of core 1 O-glycans in the intestinal epithelium (TM-IEC C1galt1 /–) also develop spontaneous colitis.
Taken together, these data indicate that deficiency in core circadian component, BMAL1, affects not only rhythmicity in locomotor activity, but other patterns of behavior as well.
The relative weaknesses are as follows: (1) the overall underdeveloped strength of enterprises, with inherent deficiencies in their core competitiveness and innovation levels; (2) lack of certain core technologies; (3) lack of a sophisticated standardization and incomplete standards system; and (4) weak brand-building ability and insufficient brand promotion.
For example, mutations or deficiencies in core clock genes such as Clock or Bmal1 result in obesity, lipodystrophy and/or glucose homeostasis abnormalities [5], [6], [7], [8], [9], and nuclear receptors central to regulating metabolic processes, such as PPARα and PGC-1α, affect the circadian clock [10], [11].
These observations suggest an inherent deficiency in the core components involved in the G2/M progression in the O2 insensitive cell lines.
Furthermore, the sensitivity of rfs-1 animals to IR is relatively weak compared to deficiency in the core HR component BRC-1, whereas sensitivity of rfs-1 and brc-1 animals to crosslinking agents is virtually indistinguishable, in support of the greater specificity of RFS-1/RIP-1 toward stalled replication fork substrates (Ward et al., 2007).
