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J R Litaker

Publications and source records attributed to J R Litaker.

3 recordsLinked to original sources

A confirmatory factor analysis evaluation of the coronary heart disease risk factors of metabolic syndrome with emphasis on the insulin resistance factor.

AIM: The goals of this study were: (1) to analyse the underlying associations between coronary risk factors and the metabolic syndrome and (2) to evaluate the construct validity of the variables used to measure each factor. METHODS: The subjects were from a previously studied cohort of 284 middle-aged Caucasian males from Goteborg, Sweden, who were selected from the National Population Register. A confirmatory factor analysis was performed using EQS Multivariate Software Version 5.7b with maximum likelihood estimation. Hypertension, obesity, insulin resistance and hyperlipidaemia were the latent factors hypothesized. RESULTS: The final, four-factor model showed good fit, with significant intercorrelations noted between all factors. The highest correlations were noted between the insulin resistance factor and the obesity factor (r = 0.887) and the insulin resistance factor and the lipid factor (r = 0.835). All factors exhibited good values for construct reliability and variance extracted except for the insulin resistance factor, which was measured with the variables of fasting insulin and fasting glucose levels. CONCLUSIONS: A four-factor model of metabolic syndrome including the coronary heart disease risk factors of hypertension, obesity, insulin resistance and hyperlipidaemia was developed using this sample of European, middle-aged Caucasian males. Insulin resistance was not well defined using the variables of fasting insulin and fasting glucose levels. Other possible variables to include in the measurement of this factor are discussed.

Anthropometry↗

Expression profile of senescence-associated beta-galactosidase and activation of telomerase in human ovarian surface epithelial cells undergoing immortalization.

Senescence is a specific physiological stage of cells characterized by long population doubling time. It accounts for the inability of normal somatic cells to undergo indefinite cell division. As the number of population doublings increase, cell cycle regulatory mechanisms come into play and signal cells to exit the cell cycle and become senescent. Senescence has been implicated in the aging process and may function as a tumor suppressor mechanism in human cells. The ability to measure the degree of cellular senescence is important in understanding the biological processes regulating cell aging and immortalization. Senescent cells exhibit an enzyme termed senescence-associated histochemical staining. Cells immortalized by viral oncogenes often enter a stage of crisis at the early phase of immortalization. The cells at crisis have a long population doubling time. Cells at the crisis stage resemble senescent cells and the expression of SA- beta-Gal may be used to monitor the process of immortalization. In this study the expression profile of SA-beta-Gal was examined in human ovarian surface epithelial cells (HOSE 6-3) undergoing immortalization by the human papilloma viral oncogene E6 and E7 (HPV E6 and E7). Our results showed a low percentage (12.0%) of HOSE 6-3 cells expressing SA-beta-Gal activity at the pre-crisis stage. The percentage of HOSE 6-3 cells expressing SA-beta-Gal activity was highest (39.2%) at the crisis stage. When HOSE 6-3 cells achieved immortalized status there was a sharp decrease in cells (1. 3%) expressing SA-beta-Gal activity. In addition, an inverse relationship between the expression of SA-beta-Gal activity and telomerase activity was noted in cells undergoing immortalization. The results confirm that the SA-beta-Gal enzyme is a good marker for monitoring the population of cells undergoing senescence at different stages of immortalization and that telomerase activation is a characteristic feature of post-crisis cells.

Biomarkers↗