Profitability and acceptability of fat- and sodium-modified hot entrees in a worksite cafeteria.

OBJECTIVES: To compare the acceptability of fat- and sodium-modified entrees before and after implementation of a marketing program and to determine the effect offering and marketing these healthful entrees had on total cafeteria and entree sales in a worksite cafeteria. DESIGN: The research was conducted in five phases, including sales data collection, acceptance testing of unmodified hot entrees, acceptance testing of modified entrees, and implementation of a marketing campaign for promoting low-fat, sodium-controlled food selections. SETTING: The Kansas Farm Bureau and Affiliated Services (KFB) employee cafeteria. SUBJECTS: KFB employees who ate lunch in the employee cafeteria and were willing to participate in the study. MAIN OUTCOME MEASURES: Sales data (percent of customers purchasing a modified entree and sales of modified entree as a percent of total sales); nutrient analysis data (energy, grams of total fat, percent of energy from fat, milligrams of cholesterol, and milligrams of sodium); and acceptability data (11 characteristics were measured using a seven-point hedonic scale). STATISTICAL ANALYSIS PERFORMED: General linear model analysis of variance was used to compare sales data from phases 1 to 5 and to compare acceptability data from phases 2 to 4. RESULTS: No significant differences in sales data were observed during the 7-month study. No significant changes in overall acceptability were found for any entree. However, customers tended to rate overall acceptability higher when entrees were marketed as lower in fat and sodium. APPLICATIONS/CONCLUSIONS: Customers in worksite cafeterias may be more willing to tolerate changes in flavor attributes when modified entrees are marketed as "healthful" and nutrition information is available.

Can academic medical centers compete in a managed care system?

The authors review characteristics of successful group practices, health maintenance organizations, and integrated service networks and then identify the critical actions that academic medical centers must take in order to compete with such service-oriented community providers. Centers must (1) form the clinical faculty into a competitive medical group that offers more price-competitive and user-friendly services; (2) restructure clinical training to be more relevant to the emerging practice situation; and (3) clearly delineate funding streams and identify the cross-subsidies taking place in the teaching, research, and patient care enterprises. These changes have the potential to strengthen clinical training and improve the financial positions of both the faculty and the university hospitals. The authors maintain that centers can make these and other necessary changes while still providing high-quality care and maintaining their educational and research functions; they cite organizations that have succeeded in these ways. However, as with all complex, large-scale organizations, public and private alike, the major factor limiting centers' ability to make the organizational changes required to successfully compete in the new health care environment is the lack of political will. It will be very difficult for academic medical centers to unite their powerful internal interest groups and take action without first experiencing a rather severe external jolt. The challenge for the leaders of academic medical centers is to prepare for the managed care jolt so that they can then guide their institutions to a new, more competitive position.

Cellular pharmacology of chloroquinoxaline sulfonamide and a related compound in murine B16 melanoma cells.

Chloroquinoxaline sulfonamide (CQS), a chlorinated derivative of sulfaquinoxaline (SQ), inhibited proliferation of murine B16 melanoma cells, but only when relatively high drug concentrations (1 mM) were used. The inhibition of cell growth by CQS was at least partially reversible by incubation in drug-free medium. Incubation of melanoma cells with CQS was associated with an arrest of the cell cycle in G0/G1 as measured by flow cytometry. The drug slightly decreased uptake of radiolabeled deoxyuridine and thymidine after 24- and 48-hr incubation periods but increased nucleoside incorporation at 72 hr. No evidence of intercalation with DNA was found. Because SQ previously was reported to inhibit an aspect of folate metabolism, we investigated the possibility that CQS limits tumor cell growth by altering folate homeostasis. This appears unlikely, however, in view of the following observations: (1) the cytotoxic effects of CQS could not be reversed by folinic acid; (2) deoxyuridine suppression of thymidine incorporation was not affected by CQS treatment; (3) CQS did not inhibit dihydrofolate reductase from mammalian or bacterial sources; and (4) CQS toxicity in mice was not reduced by folinic acid. Experiments performed with analogues modified in the quinoxaline and para-amino phenyl functions indicated that tumor cell inhibition did not require preservation of the conventional sulfonamide structure.

Effects of folate deficiency on the metastatic potential of murine melanoma cells.

Experiments were designed to measure the effect of folic acid deficiency on a major determinant of cancer lethality, the propensity to form metastases. Murine B16 melanoma cells (F10 strain) were grown in folate-deficient and -supplemented media. After 3 days, cells in the deficient medium had restricted proliferative capacity, low folate levels by bioassay, increased cell volume, abnormal deoxyuridine suppression tests, accumulation of cells in S phase by flow cytometry, and increased numbers of DNA strand breaks. These folate-deficient cells consistently initiated more pulmonary metastases than control cells when injected into host mice. Cell size did not appear to be a major factor in pulmonary metastasis formation. In vitro growth rates and cloning efficiencies were comparable for cells in both types of medium as was subcutaneous growth of tumors. We conclude that folate deficiency increases the metastatic potential of cultured melanoma cells.

Inhibition of lymphocyte nucleic acid metabolism and antibody production by trimetrexate.

Trimetrexate is a lipid soluble dihydrofolate reductase inhibitor which, unlike methotrexate, does not depend upon the membrane folate transport system for cell entry. We investigated the possibility that trimetrexate (but not methotrexate) might permeate intermitotic lymphocytes and, following stimulation, impair only the responding cells, rather than all dividing cells, as is the case with methotrexate. Peripheral blood mononuclear cells from normal individuals were incubated for 1 hr in three moderate to high concentrations (1, 10 and 100 microM) of methotrexate or trimetrexate, washed, and incubated with phytohemagglutinin. Intracellular folate activity, as assessed by the deoxyuridine suppression test, was abnormal at all three concentrations of trimetrexate but only at the highest concentration of methotrexate. Similarly, incorporation of [3H]deoxyuridine was depressed profoundly in trimetrexate-treated cells (2% of control) but unaffected by methotrexate. Analysis of cell cycle distribution by flow cytometry confirmed G0 + G1 arrest in trimetrexate but not methotrexate-treated cells. Neither drug altered morphologic transformation, Tac antigen expression, or incorporation of [3H]thymidine by the "salvage" pathway. Therefore, brief exposure to methotrexate has little effect on intermitotic lymphocytes, whereas trimetrexate very specifically inhibits the conversion of deoxyuridine to thymidine in these cells and leads to the arrest of DNA synthesis in the G0 + G1 phase. This metabolic abnormality markedly reduces in vitro antibody synthesis: a 1-hr treatment of lymphocytes with 10 or 100 microM trimetrexate prior to incubation with pokeweed mitogen on four occasions completely inhibited both IgG and IgM secretion. Similar treatment with methotrexate had no effect until the highest concentration (100 microM) was used. We conclude that brief exposure of peripheral blood mononuclear cells to the nonclassical dihydrofolate reductase inhibitor, trimetrexate, results in inhibition of nucleic acid synthesis and impairment of antibody production. This drug effect may permit more incisive modulation of immune responses.

Dietary fiber constituents of selected fruits and vegetables.

This study compared the dietary fiber (DF), neutral detergent fiber (NDF), cellulose, hemicellulose, lignin, and pectin content of selected fruits and vegetables. Apples and peaches (fresh and canned), oranges (fresh), strawberries (fresh, canned, and frozen), carrots, green beans, and potatoes (fresh, fresh cooked, canned, and frozen), and tomatoes (fresh, fresh cooked, and canned) were studied. When possible, two varieties, two stores, and name and store brands were chosen. Samples were analyzed for NDF, acid detergent fiber, 72% sulfuric acid, lignin, and pectin. From those values, DF, cellulose, and hemicellulose were calculated. Fresh fruits in gm/100gm wet weight had decreasing DF, NDF, and hemicellulose values as follows: apples, peaches, strawberries, and oranges. Apples were highest in cellulose; strawberries, highest in lignin; and oranges, highest in pectin. Fresh-cooked vegetables in gm/100gm wet weight have decreasing DF and NDF values as follows: green beans, carrots, potatoes, and tomatoes. Green beans were highest in cellulose and hemicellulose; potatoes highest in lignin; and carrots highest in pectin. On a wet-weight basis, fresh apples and peaches, fresh-cooked green beans, canned carrots, and canned and frozen potatoes were higher in DF and NDF than other forms of the fruit or vegetable. There were few differences according to stores, brands, or varieties of fruits and vegetables. On a dry-weight basis, fresh apples, peaches, strawberries, green beans, and tomatoes appear to have higher DF and NDF contents than their processed counterparts. Fresh-cooked carrots and fresh potatoes appear to have less DF and NDF than their canned and frozen counterparts.