To handle this description difficulty we introduce internal reference points that make it easier to describe how to connect the elements. So try this claim: In fact, in dependent claims you build on a claim earlier to narrow the description to make it more specific.
That gave encouragement to others that rigorous experimental work addressing brain-behavior relations was possible in infants. It also fundamentally altered the scientific understanding of PFC early in development; clearly it was not silent as accepted wisdom had held. Even though PFC is very immature early in life and takes a very long time to develop, it can already subserve elementary versions of the highest cognitive functions during the first year of life.
Diamond went on to facilitate many of the earliest collaborations between developmental and cognitive scientists, on the one hand, and neuroscientists on the other.
She provided the first demonstration of a visual deficit in treated PKU children which changed international guidelines for the age of treatment onset. No one had ever done anything like that.
Again, the answer lay in integrating two fields. Neuropharmacologists studying the mesocortical dopamine system in rats had shown that if there is only a modest reduction in the dopamine precursor, tyrosine, PFC is selectively affected. To test that hypothesis, Diamond again turned to work in both humans and animals.
They were thereby able to demonstrate the mechanism causing the deficits that had so confounded those working in inborn errors of metabolism, and to demonstrate that the deficits could be prevented by stricter dietary restrictons.
Midway through, Diamond learned that the dopamine system in the retina shares the same unusual properties as those that cause PFC to be sensitive to reductions in available tyrosine too small to affect other brain regions.
To be consistent, she had to predict that retinal function would also be adversely impacted in children treated for PKU, so she ventured into vision science to investigate that together with pediatric optometrist, Dr.
Two superficially unrelated behavioral effects a selective cognitive deficit and a selective visual deficit were found to have same underlying cause.
An animal model of early-treated PKU. Journal of Neuroscience, 14, Diamond, A. Impaired sensitivity to visual contrast in children treated early and continuously for PKU. Prefrontal cortex cognitive deficits in children treated early and continuously for PKU. Cognitive deficits in a genetic mouse model of the most common biochemical cause of human mental retardation.
Journal of Neuroscience, 19, A model system for studying the role of dopamine in prefrontal cortex during early development in humans. Reprinted in Reader in brain development and cognition. One discrepancy troubled Diamond, however. The visual deficits were not.
By the time her team studied contrast sensitivity, they knew what range of Phe levels produced a deficit and so only sampled from within that range. Having a truncated range of current Phe levels could easily have accounted for the failure to find a relation between contrast sensitivity and current Phe levels.
However, a child born with PKU is usually not started on treatment for the disorder until about 10 days of age. The visual system is maturing very rapidly during the days and weeks right after birth.
Perhaps the excessively high levels of Phe reaching the brain during those first days after birth impairs the visual system. To test that hypothesis Diamond brought in pairs of siblings, both of whom had PKU, as well as children from the general population.
The importance of the sibling pairs was that while PKU in the first child born with the disorder is not detected until the heel prick test after birth, amniocentesis is performed for all later-born children and so it is known if any of those children have PKU before birth.
The first-born children started dietary treatment on average at 11 days of age, while the later-born children started the diet on average at 3 days of age. They found consistently that the first PKU sibling in a family had poorer contrast sensitivity at low levels of contrast than his or her younger PKU sibling and than children from the general population.
The children whose brains were exposed to massive levels of Phe for the first 10 days of life showed no deficits in visual acuity or in determining form from texture, but they were impaired in contrast sensitivity at very low levels of contrast and in determining form from motion.
These deficits were evident over 10 years later when we tested the children. This is in striking parallel to the findings of Daphne Maurer and Terri Lewis who have found that children exposed to very degraded visual input for only the first few weeks after birth children born with congenital cataracts who received surgery to correct their eyesight within the first month of life.
Evidently, there is still some role for current Phe levels in the contrast sensitivity deficit of PKU children, as high Phe levels during the first 10 days of age are related to deficits only at very low contrast, but PKU children have impaired contrast sensitivity across spatial frequencies and levels of contrast.
Both neonatal and current Phe levels appear to matter. Recent research findings on the effects of age at diet initiation on the visual system. Consequences of variations in genes that affect dopamine in prefrontal cortex. Cerebral Cortex, 17, Scientific results are rarely perfectly neat and clean.
Diamond had predicted that performance on all tasks dependent on PFC would be impaired in PKU children with mildly elevated Phe levels. Why on earth were they not impaired on these 3 tasks?As with your other application materials, your writing sample must be error-free.
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