The consistency of change in the development of nursing faculty practice plans.

Nursing faculty practice plans need to be inherently flexible to meet the changing needs of nursing schools and the external clients of the practice plans. The University of Texas-Houston Health Science Center (UT-Houston) School of Nursing has constructed two integrated models of faculty practice to meet the challenges of change. Our linkage model with outside agencies and our academic nursing center provided in excess of one million dollars of support to the School of Nursing in fiscal year 1992-1993. Flexibility in our linkage model is discussed in such areas as the negotiation process for contracts with outside agencies, methods of payment for services, calculations of cost recoveries, methods of setting consultant rate levels, revisions of fund-disbursement policies, and development of fund-tracking systems. UT-Houston School of Nursing's nursing center model is based on a business plan and was established without outside funding assistance. Over time, the areas of concentration have changed because of changing community needs and market conditions. Its revenues depend on marketing efforts by the clinic staff. Evaluation and outcome research, to be based on computerized financial and patient record information systems, are considered critical elements in maintaining the UT-Houston cutting-edge leadership as an academic nursing center.

Nursing centers: service as a business.

In 1988 The University of Texas Houston Health Science Center School of Nursing embarked on the task of developing a nursing center (UTNS). Today the organization is in excellent financial health and its patient population continues to grow. The UTNS model can help nursing centers move forward as a prototype of primary health care delivery.

The Houston Linkage Model 1992; an update.

The authors provide an update on the development of an innovative model to promote faculty practice. Since its inception, the model has become more sophisticated and has more than tripled its revenues to the school of nursing. Faculty practice is an integral part of the teaching programs and has been the impetus for increased research productivity among faculty members. The authors discuss model changes, including the management of revenues and decentralized control of funds.

Role of ornithine decarboxylase in functional development of rat gastric mucosa.

The effects of inhibiting polyamine synthesis on the functional development of the gastric mucosa were studied in rats from 5 to 40 days old. They were treated from day 14 after birth with alpha-difluoromethylornithine (DFMO) at a concentration of 2% in the drinking water of mothers and pups. The rats were weaned on day 18. Basal acid and pepsin secretion, oxyntic gland mucosal pepsinogen content, and antral gastrin content followed similar developmental patterns in control animals. Levels of these parameters remained measurable but low until around the time of weaning, when dramatic log linear rises were observed. DFMO failed to delay the onset of the rises in any of these maturational indices. Ornithine decarboxylase (ODC) activity in the oxyntic gland mucosa was low but discernible in rats of every age studied. DFMO significantly reduced ODC activity at every age except 40 days, where there was no difference from control values. Our results suggest that ODC activity in the rat gastric mucosa does not change appreciably during neonatal development and that inhibiting putrescine synthesis from its precursor ornithine by DFMO treatment does not prevent or delay gastric mucosal maturation.

Stimulation of growth of a colon cancer cell line by gastrin.

The trophic effects of the hormone gastrin-17 were examined on a human colon cancer cell line. LoVo cells were obtained from the American Type Culture Collection and grown in minimal essential medium in the presence of 10% bovine fetal serum. To demonstrate the trophic effect of gastrin, synchronization was necessary. The effect of gastrin was optimal after 26-h exposure to 0.6 mM thymidine. In the presence of serum the optimal dose of gastrin for stimulation of DNA synthesis was 7.2 X 10(-10) M. Under these conditions gastrin caused a 220% increase in [3H]thymidine incorporation. In the absence of serum the optimal dose of gastrin (3.6 X 10(-9) M) increased DNA synthesis approximately 200%. Twenty-four hours after gastrin treatment (1.8 X 10(-10) M gastrin 17) cell numbers increased 50.8% compared with control. At 48 h this increase was maintained at 44%. Maximum stimulation by gastrin occurred 7-8 h after release from synchronization and exposure to gastrin. This corresponded to the S phase of the cell cycle. Significant stimulation occurred a second time at 22-24 h, presumably during the second S phase in a still synchronous or partially synchronous cell population. These data demonstrate that physiological concentrations of gastrin-17 can stimulate the growth of a human cancer cell line and that some degree of synchronization may be necessary to demonstrate similar effects in other cell lines. Such cell lines may provide a source of rapidly growing cells in which the mechanisms of the trophic effect of gastrin can be examined.

Effects of sodium warfarin and sodium heparin plus anticancer agents on growth of rat C6 glioma cells.

The effects of racemic sodium warfarin (warfarin) and sodium heparin (heparin) on brain tumor cells were assessed in the rat C6 glioma cell line. After anticoagulant treatment lasting up to 5 days, cell growth was not inhibited by warfarin at low doses (10(-4) to 10(-5) M), but both cell growth and cellular adherence to culture plates were inhibited at high doses (10(-3) to 10(-2) M). Sodium heparin, even at high doses, did not affect cell growth or adherence. Warfarin (10(-3) M) significantly decreased and heparin (12.6 U/ml) had no effect on [3H]thymidine and [14C]leucine incorporation after 3- or 24-hour anticoagulant treatment. Colony formation studies examined the effects of 24-hour warfarin (10(-3) M) or heparin (12.6 U/ml) pretreatment plus a 2-hour incubation with one of seven anticancer agents. Supra-additive toxic effects were produced by warfarin plus chlorambucil, heparin plus chlorambucil, heparin plus carmustine, and heparin plus teniposide. At low doses of warfarin (10(-5) M) or heparin (0.126 U/ml), heparin plus carmustine and heparin plus teniposide remained synergistic.

The bioavailability of oral and intravenous ifosfamide in the treatment of bronchogenic carcinoma.

This study tested the feasibility of using oral ifosfamide to treat bronchogenic carcinoma and compared the pharmacokinetics of intravenous and oral doses of the drug. Patients with advanced bronchogenic carcinoma were evaluated for toxicities associated with oral ifosfamide therapy. Pharmacokinetics for various oral and intravenous doses of ifosfamide were determined by a gas-liquid chromatographic assay of plasma and urine samples. Toxicities associated with oral ifosfamide therapy were minimal. Calculated pharmacokinetics parameters are listed, with the half-lives varying from 0.5 to 4.6 h. Oral ifosfamide therapy was determined to be feasible, and further studies are justified to assess the pharmacokinetics of the optimum dosage and scheduling regimens.