PubMed Health⌕ Search

Biomedical subjects

Robert Payne

Publications and source records attributed to Robert Payne.

2 recordsLinked to original sources

Transformations of mathematical and stimulus functions.

Following a pretest, 8 participants who were unfamiliar with algebraic and trigonometric functions received a brief presentation on the rectangular coordinate system. Next, they participated in a computer-interactive matching-to-sample procedure that trained formula-to-formula and formula-to-graph relations. Then, they were exposed to 40 novel formula-to-graph tests and 10 novel graph-to-formula tests. Seven of the 8 participants showed substantial improvement in identifying formula-to-graph relations; however, in the test of novel graph-to-formula relations, participants tended to select equations in their factored form. Next, we manipulated contextual cues in the form of rules regarding mathematical preferences. First, we informed participants that standard forms of equations were preferred over factored forms. In a subsequent test of 10 additional novel graph-to-formula relations, participants shifted their selections to favor equations in their standard form. This preference reversed during 10 more tests when financial reward was made contingent on correct identification of formulas in factored form. Formula preferences and transformation of novel mathematical and stimulus functions are discussed.

Adult↗

Wnk1 kinase deficiency lowers blood pressure in mice: a gene-trap screen to identify potential targets for therapeutic intervention.

The availability of both the mouse and human genome sequences allows for the systematic discovery of human gene function through the use of the mouse as a model system. To accelerate the genetic determination of gene function, we have developed a sequence-tagged gene-trap library of >270,000 mouse embryonic stem cell clones representing mutations in approximately 60% of mammalian genes. Through the generation and phenotypic analysis of knockout mice from this resource, we are undertaking a functional screen to identify genes regulating physiological parameters such as blood pressure. As part of this screen, mice deficient for the Wnk1 kinase gene were generated and analyzed. Genetic studies in humans have shown that large intronic deletions in WNK1 lead to its overexpression and are responsible for pseudohypoaldosteronism type II, an autosomal dominant disorder characterized by hypertension, increased renal salt reabsorption, and impaired K+ and H+ excretion. Consistent with the human genetic studies, Wnk1 heterozygous mice displayed a significant decrease in blood pressure. Mice homozygous for the Wnk1 mutation died during embryonic development before day 13 of gestation. These results demonstrate that Wnk1 is a regulator of blood pressure critical for development and illustrate the utility of a functional screen driven by a sequence-based mutagenesis approach.

Animals↗