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Daniel L. Cook

Researcher at University of Washington

Publications -  71
Citations -  4981

Daniel L. Cook is an academic researcher from University of Washington. The author has contributed to research in topics: Biosimulation & Ontology (information science). The author has an hindex of 33, co-authored 71 publications receiving 4812 citations. Previous affiliations of Daniel L. Cook include Veterans Health Administration & United States Department of Veterans Affairs.

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Intracellular ATP directly blocks K + channels in pancreatic B-cells

TL;DR: During patch–clamp studies of proton inhibition of Ca2+-activated K+ channels in B-cells, a second K+-selective channel is identified which is rapidly and reversibly inhibited by ATP applied to the cytoplasmic surface of the membrane.
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Differential changes of autonomic nervous system function with age in man.

TL;DR: It is concluded that autonomic nervous system function also declines with aging, but that other age-related changes such as a decline of baroreceptor sensitivity may lead to compensatory autonomics nervous system response, which could mask underlying functional defects.
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Quantitative Evaluation of Cardiac Parasympathetic Activity in Normal and Diabetic Man

TL;DR: It is concluded that supine RR variation during a deep respiratory rate and during β-adrenergic blockade is a sensitive, quantitative, and reproducible method to evaluate parasympathetic nervous activity in normal and diabetic subjects and cardiac parASYmpathetic activity may be diminished in diabetic subjects before clinical symptoms of autonomic neuropathy are evident.
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Autonomic Neural Dysfunction in Recently Diagnosed Diabetic Subjects

TL;DR: It would appear that the ANS is impaired soon after the diagnosis of diabetes mellitus, consistent with the hypothesis that abnormal carbohydrate metabolism is an important factor in the etiology of diabetic autonomic neuropathy.
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Modeling stochastic gene expression: Implications for haploinsufficiency

TL;DR: It is suggested that null mutations of a single allele in a diploid organism could decrease the probability of gene expression, and the hypothesis that some haploinsufficiency syndromes might result from an increased susceptibility to stochastic delays of gene initiation or interruptions of geneexpression is presented.