A pilot study of the cost of educating undergraduate medical students at Virginia Commonwealth University.

PURPOSE: To develop a model isolating the annual per-student cost of, and the fund sources for, educating undergraduate medical students at the Virginia Commonwealth University Medical College of Virginia School of Medicine. METHOD: For 1994-95, hours that faculty spent in direct scheduled contact with students and time that students spent in direct scheduled contact with faculty were inventoried. Student, faculty, and resident contact hours for clinical clerkships and electives were estimated. Faculty contact hours and average faculty workload profiles were used to compute the number of full-time-equivalent faculty positions required to deliver the undergraduate medical curriculum. Support staff and operating budget requirements were based on the number of required faculty, and actual salary averages were used to compute faculty and staff costs. Other institutional costs that indirectly support undergraduate medical education were estimated. Using faculty contact hours and actual cost data, fund sources that support undergraduate medical education were identified. RESULTS: Medical school faculty spent more than 89,000 scheduled hours teaching 674 undergraduate medical students. The faculty-student ratio was 1:3.35. Residents spent nearly 79,000 hours training undergraduate medical students. The total annual cost of undergraduate medical education was $69,992 per student. State funds contributed less than a third of the required financial resources; faculty clinical practice funds provided nearly half. CONCLUSION: Although there are inherent complexities, isolating the cost and fund sources of undergraduate medical education is an essential first step toward providing categorical funding. The model developed during the study provides a basis for assigning costs, allocating resources among instructional programs, and predicting incremental costs (or savings) and revenue requirements. The model may be of use to other medical schools contemplating new strategies for financing undergraduate medical education.

Position 2 and position 2/Ala15-substituted analogs of bovine growth hormone-releasing factor (bGRF) with enhanced metabolic stability and improved in vivo bioactivity.

In order to prepare GRF analogs with high activity in vivo, a strategy was undertaken to stabilize the peptide to dipeptidylpeptidase IV (DPP-IV), a protease found in plasma which inactivates native human and bovine GRF by cleavage of the Ala2-Asp3 bond. Replacement of the Ala2 residue with Ser, Thr, or Gly in [Leu27]bGRF(1-29)NH2 resulted in peptides greatly stabilized against proteolysis in plasma, but having low inherent GH-releasing activity when tested in bovine pituitary cell cultures. Replacement of Gly15 with Ala15 was marginally effective in improving the in vitro bioactivity of this group of peptides. When tested for GH-hormone release in steers, however, the Thr2,Ala15 analog was four times more potent than bGRF(1-44)NH2. Eleven additional analogs from the [X2,Ala15,Leu27]bGRF(1-29)NH2 series were synthesized and evaluated for metabolic stability in bovine plasma and for GH releasing activity in steers in vivo and in rat pituitary cells in vitro. Two compounds, [Val2,Ala15,Leu27]dGRF(1-29)NH2 and [Ile2,Ala15,Leu27]-bGRF(1-29)NH2, had increased GH-releasing activity in steers over that of [Thr2,Ala15,Leu27]-bGRF(1-29)NH2 and over a previously reported super-potent analog, [desNH2Tyr1,D-Ala2,Ala15]-hGRF(1-29)NH2.

Recombinant bovine somatotropin improves growth performance in finishing beef steers.

The objectives of this study were to determine the efficacy of various doses of rbST on ADG and feed efficiency (FE) and to describe carcass composition changes in finishing beef steers. In Exp. 1, 96 crossbred beef steers (393 kg) received daily i.m. injections of buffer or 33, 100, or 300 micrograms/kg of BW of rbST (0ST, 33ST, 100ST, 300ST). In Exp. 2, 200 crossbred beef steers (417 kg) received daily i.m. injections of buffer or 8.25, 16.5, 33, or 66 micrograms/kg of BW or rbST (0ST, 8.25ST, 16.5ST, 33ST, 66ST). Treatments were administered until steer BW per pen averaged 540 kg in Exp. 1 and 560 kg in Exp. 2. An 86% concentrate: 14% roughage diet was fed once daily (CP: 16.5% in Exp. 1, 20.2% in Exp. 2). In Exp. 1, growth performance of steers receiving rbST was dose-dependent; ADG changed linearly (P = .01), DMI decreased linearly (P = .03), and FE changed quadratically (P less than .03). The 33ST steers responded with improved ADG and FE, 100ST with improved FE, and 300ST with lower ADG and poorer FE, compared with 0ST. In Exp. 2, the ADG response was quadratic (P = .01), DMI decreased linearly (P = .003), and FE improved quadratically (P = .004) with increasing dose of rbST. Steers receiving 16.5ST and 33ST responded with improved ADG and FE, whereas steers receiving 8.25ST and 66ST responded with improved FE but not ADG relative to 0ST steers. In Exp. 1 and 2, rbST administration altered carcass composition by increasing carcass protein and decreasing carcass fat.(ABSTRACT TRUNCATED AT 250 WORDS)

LH and FSH response of Holstein heifers to fertirelin acetate, gonadorelin and buserelin.

This study was conducted to describe the changes in serum LH and FSH concentrations in Holstein heifers following intramuscular (i.m.) injection of various dosages of fertirelin acetate and other commercially available GnRH products at their labeled dosages. The design was an incomplete Latin-square which gave nine replicates of each treatment. Treatments administered on Days 8 to 16 of the estrous cycle consisted of saline; 25, 50, 100 or 200 microg fertirelin acetate; 100, 250 or 500 microg gonadorelin; and 10 or 20 microg buserelin. Blood samples were collected via jugular catheters from 1 h before to 8 h after each injection. Log (Base 2) area under the LH and FSH curves (log AUC) were used to evaluate response to fertirelin acetate dosages and to determine difference (LSD: 0.05) and bioequivalence (alpha = 0.05) between the various dosages of GnRH products tested. Significant quadratic dose response relationships were detected for the LH and FSH log AUC data. Plots of the LH log AUC but not the FSH log AUC data suggested that a response plateau was being approached at the higher dosages of fertirelin acetate. Bioequivalence (alpha = 0.05) was based on the assumption that two means are equivalent if they differ by no more than 20% of the reference log AUC mean. Using these criteria fertirelin acetate is 2.5 to 10 times more potent than gonadorelin, whereas buserelin is approximately 10 to 20 times more potent than fertirelin acetate in the bovine for LH and FSH release.