Biomedical subjects

D A Ralph

Publications and source records attributed to D A Ralph.

3 recordsLinked to original sources

PubMed1992

Transforming growth factor-beta.

This chapter has described some of the most salient features of the biology of the TGF-beta s. The TGF-beta s are of great interest as growth inhibitors, regulators of cell phenotype and regulators of cell adhesion. The various TGF-beta isoforms are highly conserved and display a complex pattern of interactions with multiple membrane receptor components. Activation of these receptors leads to inhibition of epithelial cell proliferation by a mechanism that may involve proteins related to the growth suppressor, RB. TGF-beta receptors are also coupled to mechanisms that control expression of differentiation commitment genes and differentiated cell functions. TGF-beta can affect cell proliferation and differentiation through indirect mechanisms involving regulation of expression of cytokines, extracellular matrix molecules and their respective receptors. These responses strongly influence the growth and phenotype of an array of cell types. Excess or reduced TGF-beta activity may contribute to the pathogenesis of certain fibrotic disorders and certain hyperproliferative disorders including cancer, respectively.

Cell Differentiation↗

PubMed1991

Early gene responses to transforming growth factor-beta in cells lacking growth-suppressive RB function.

The growth-suppressive function of the retinoblastoma susceptibility gene product, RB, has been implicated in the mediation of growth inhibition and negative regulation of certain proliferation related genes by transforming growth factor-beta 1 (TGF-beta 1). Early gene responses to TGF-beta 1 were examined in order to determine their dependence on the cell cycle and on the growth-suppressive function of RB. TGF-beta 1, which rapidly elevates the steady-state level of junB and PAI-1 mRNAs and decreases that of c-myc mRNA, induces these responses in S-phase populations of Mv1Lu lung epithelial cells containing RB in a phosphorylated state. Since in this state RB is presumed to lack growth-suppressive activity, the response to TGF-beta 1 was also examined in DU145 human prostate carcinoma cells whose mutant RB product lacks growth-suppressive function. In these cells, TGF-beta 1 also decreases c-myc expression at the transcription initiation level. These results suggests that the c-myc, junB, and PAI-1 responses to TGF-beta 1 are not restricted to the G1 phase of the cell cycle and that down-regulation of c-myc expression by TGF-beta 1 can occur through a mechanism independent from the growth-suppressive function of RB.

Animals↗

PubMed1987

Oklahoma pharmacists' explanations of professional satisfaction and dissatisfaction.

This study examined whether the theoretical constructs of role conflict and incomplete professionalization serve as valid explanations of pharmacists' professional satisfaction or dissatisfaction. A sample of registered pharmacists in Oklahoma responded to a mail-out questionnaire containing indicies designed to measure job satisfaction and professional satisfaction. The questionnaire also included a satisfaction inventory of 17 facets considered to characterize pharmacy as a profession. From the questionnaire respondents, samples of pharmacists demonstrating extreme professional satisfaction and extreme dissatisfaction were randomly selected for telephone interviews. This study found pharmacists' professional satisfaction to be significantly less than satisfaction with their job. The study results would indicate that incomplete professionalization and internalized career goals rather than role conflicts are significantly related to pharmacist professional satisfaction.

Conflict, Psychological↗