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J S Cowen

Publications and source records attributed to J S Cowen.

6 recordsLinked to original sources
PubMed1994

Errors and bias in using predictive scoring systems.

Scoring systems used to predict clinical outcomes for critically ill patients have been refined in the past decade, yet even the most recently developed systems contain flaws that limit their application. In general, prediction rules are derived by defining an association between a number of clinical variables and a particular outcome in a reference patient population. By systematically examining the qualities of the independent variables and the size and scope of the derivation data set, potential sources of error and bias can be identified. Existing and future predictive systems must be validated on large groups of patients and continuously updated to keep pace with new approaches to the practice of critical care medicine.

Bias↗
PubMed1983

Comparison of Trembler and Trembler-J mouse phenotypes: varying severity of peripheral hypomyelination.

Trembler (Tr) is an autosomal dominant mutation which produces hypomyelination and demyelination in the mouse peripheral nervous system. This paper compares the genetic, behavioral, and pathological aspects of trembler-J, (TrJ) to those of the original Tr mutation. We found that TrJ was tightly linked on chromosome 11 to vestigial tail, vt, as is Tr. Most TrJ/? animals were more mildly affected behaviorally and pathologically than Tr/? animals. Tr/? animals were rather uniformly affected. In contrast, with matings of mildly affected TrJ/? (putative TrJ/+) animals to each other, and not with matings of putative TrJ/+ X +/+, some offspring, putative homozygotes, TrJ/TrJ, were more severely affected behaviorally and had more extreme peripheral hypomyelination than any Tr/? animals. In spite of their differences, Tr/?, putative TrJ/+, and putative TrJ/TrJ animals shared a failure or marked delay of Schwann cells to progress from the stage of axonal ensheathment in a 1:1 relationship to myelination. We conclude that Tr and TrJ are probably allelic, and that despite their phenotypic differences, their actions are fundamentally similar. While Tr is a dominant, we believe that TrJ behaves as a semidominant, which in homozygotes, TrJ/TrJ, produces the most severe heritable peripheral myelin deficiency hitherto described.

Alleles↗
PubMed1977

Effect of cortical spreading depression on audiogenic seizure priming of C57BL/6 mice.

At 19 days of age, C57BL/6Bg mice received KCl-induced cortical spreading depression during which they were acoustically primed by exposure to an initial auditory stimulus. At 28 days of age, the mice were tested for susceptibility to audiogenic seizures. Cortical spreading depression had no effect on acoustic priming of C57BL/6Bg mice and it had been previously reported to have no effect on acoustic priming of SJL/J mice. These findings are discussed in the context of pharmacogenetic differences for the effects of aminooxyacetic acid on acoustic priming of C57BL/6 and SJL/J mice.

Acoustic Stimulation↗
PubMed1977

Pharmacogenetic differences in audiogenic seizure priming of C57BL/6Bg and DBA/1Bg-asr mice.

Susceptibility to audiogenic seizures can be induced in some strains of resistant mice by exposure to an initial auditory stimulus (acoustic priming). Aminooxyacetic acid, hydrazine, glutamic acid, gamma-aminobutyric acid (GABA), cycloheximide, and metyrapone antagonize the acoustic priming of audiogenic seizure susceptibility in C57BL/6Bg mice, whereas only metyrapone attenuates that of DBA/1Bg-asr mice. The strain difference in the effect of AOAA and cycloheximide is correlated with a small, transient fall in level of brain GABA in C57BL/6Bg but not DBA41Bg-asr mice. These findings support our hypothesis that there are at least two neural mechanisms of acoustic priming, each with its own genetic basis and that corticosteroids are required by both mechanisms for the development of primed seizures.

Acoustic Stimulation↗