PubMed Health⌕ Search

Biomedical subjects

J K Baldwin

Publications and source records attributed to J K Baldwin.

7 recordsLinked to original sources
PubMed1991

Tumor-promoting activity of ethyl phenylpropiolate.

The ability of the hyperplasiogenic irritant ethyl phenylpropiolate (EPP) to act as a tumor promoter in two-stage carcinogenesis and to stimulate cellular events commonly cited as markers of tumor promoter action was evaluated. Treatment of adult, inbred SENCAR (SSIN) mice, initiated with 7,12-dimethylbenz(a)anthracene, with 5 mg of EPP twice weekly resulted in 100% of the mice developing tumors (4.8 tumors/mouse) after 40 weeks of promotion. Treatment with 3 mg EPP (twice weekly) resulted in 52% of the mice developing tumors (0.9 tumor/mouse). This treatment regimen with EPP produces a sustained epidermal hyperplasia without being overtly toxic. In addition, a 5-mg dose of EPP induced ornithine decarboxylase activity to a level comparable to that induced by the tumor promoter phorbol 12-myristate 13-acetate (PMA): 2.3 nmol CO2/mg protein/h for EPP versus 4.5 nmol CO2/mg protein/h for PMA versus 0.04 nmol CO2/mg protein/h for acetone control. Likewise, the time course of ornithine decarboxylase induction by EPP was the same as that seen with PMA (maximum induction at approximately 6 h). Vascular permeability of the dorsal skin increased significantly in response to EPP (8 times that seen in acetone controls) and exhibited the same kinetics as that seen after exposure to PMA. Activity of protein kinase C (PKC), the cellular receptor for PMA, decreased by 75 to 95% 48 h after treatment with PMA. In contrast, EPP treatment resulted in less than a 20% decrease in PKC activity 48 h after treatment. This slight decrease in PKC activity is thought to be an indirect effect caused by the hyperproliferative and inflammatory reactions, because EPP was found to be inactive as an in vitro activator of PKC. These results indicate not only that EPP is a good tumor promoter that causes morphological and biochemical responses similar to those induced by PMA, but also that the action of EPP is apparently mediated via a mechanism that does not involve direct interaction with PKC.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1991

Quality assurance and quality control in toxicology: how might these concepts apply to epidemiology?

Quality assurance and its distinction from quality control are defined in operational terms. The historical development of standards for scientific research supporting commercialization of materials leading to the current Good Laboratory Practice (GLP) standards is briefly outlined. The application of GLPs to toxicology studies and experience in the use of these standards over a broad range of activities is also presented. This background information provides a common starting point for consideration of the development and application of similar standards for epidemiological studies.

Epidemiologic Methods↗
PubMed1991

Quality assurance for epidemiologic studies.

Quality assurance (QA) has been successfully applied to scientific disciplines such as toxicology. Experience gained in the application of QA and quality control (QC) through a formal program of compliance with Good Laboratory Practice (GLPs) regulations has been beneficial in toxicology and can be used to develop and implement a similar program in epidemiology. We focus here on the specific ways in which GLP-mandated quality assurance can be adapted and used in epidemiology and on the consequent benefits of this effort.

Cost-Benefit Analysis↗
PubMed1991

Issues in data sharing and access: an industry perspective.

Epidemiologic data sharing and access, and information sharing and access, are complex issues with no consensus within the industrial community. The purpose of this paper is to provide an introduction, as well as some personal perspectives, to the issues of data access and sharing. These perspectives include a discussion of types of data sharing, advantages and barriers to openness, and alternatives that lower the need for sharing of the raw data.

Confidentiality↗
PubMed1990

Arachidonic acid metabolism varies with the state of differentiation in density gradient-separated mouse epidermal cells.

Epidermal cells were isolated from adult inbred SENCAR (SSIN) mice and separated by density-gradient centrifugation. The cells were pooled into three fractions shown by previous work to differ in their state of differentiation and proliferative potential. The three fractions were examined for their capacity to metabolize exogenous 14C-arachidonic acid (AA) into prostaglandins (PG) and hydroxyeicosatetraenoic acids (HETE). Cells found in the upper two fractions, which are less dense, have less proliferative potential in vitro, and are more differentiated than cells in the lower more dense fraction, are much more active in producing PG from exogenous AA than are the more dense cells. This was observed in intact cells as well as cells disrupted by freeze-thawing following density separation. The same relationship was found for HETE production in that cytoplasmic preparations from the two fractions containing the less dense cells were much more active in the production of HETE than cytoplasmic preparations from the more dense fraction. The two upper fractions differed little from each other in the production of PG or HETE. These results indicate the presence of higher levels of active cyclooxygenase and lipoxygenases in fractions containing the less dense, more differentiated cells than in the fraction containing the more dense, less differentiated cells which are highly enriched for basal keratinocytes.

Animals↗