Application of the Newell liberal arts model for interdisciplinary course design and implementation.

Health professions faculty think that interdisciplinary education is critical for students pursuing careers as health care professionals. Initial attempts at interdisciplinary education by simply combining students into groups without adequate curriculum adaptation, preparation, and planning have been ineffective. Applying the liberal arts interdisciplinary model, developed by William Newell, a transdisciplinary faculty team in the College of Health Professions of the University of New England identified the course content, design, and instructional processes necessary to create an interdisciplinary elective course. The eight-step model and how it was applied to the development of an ethics course for seven different health care professional disciplines is presented. The result of this applied design approach was a course that assisted the transition of health care professional students previously accustomed to studying and working within their own discipline to communicate, cooperate, and collaborate across discipline-specific lines.

Utilization of research methodology in designing and developing an interdisciplinary course in ethics.

Development research methodology was utilized to design an interdisciplinary ethics course for students from seven disciplines: dental hygiene, nursing, nurse anesthesia, occupational therapy, physician assistant, physical therapy, and social work. Two research questions, 'What content areas should be considered for inclusion in an interdisciplinary course in Ethics?' and 'What design framework, format, or structure would best fit the content chosen?' guided the study. An interdisciplinary faculty design team conducted a comparative analysis of each of the seven discipline's codes of ethics to find common topics of interest. Further analysis then grouped these topics into eight categories of professional responsibility. The result was a fifteen-week course with validated content relevant to all disciplines.

CYP4A1 antisense oligonucleotide reduces mesenteric vascular reactivity and blood pressure in SHR.

The cytochrome P-450 4A (CYP4A)-derived arachidonic acid metabolite 20-hydroxyeicosatetraenoic acid (20-HETE) affects renal tubular and vascular functions and has been implicated in the control of arterial pressure. We examined the effect of antisense oligonucleotide (ODN) to CYP4A1, the low K(m) arachidonic acid omega-hydroxylating isoform, on vascular 20-HETE synthesis, vascular reactivity, and blood pressure in the spontaneously hypertensive rat (SHR). Administration of CYP4A1 antisense ODN decreased mean arterial blood pressure from 137 +/- 3 to 121 +/- 4 mmHg (P < 0.05) after 5 days of treatment, whereas treatment with scrambled antisense ODN had no effect. Treatment with CYP4A1 antisense ODN reduced the level of CYP4A-immunoreactive proteins along with 20-HETE synthesis in mesenteric arterial vessels. Mesenteric arteries from rats treated with antisense ODN exhibited decreased sensitivity to the constrictor action of phenylephrine (EC(50) 0.69 +/- 0.17 vs. 1.77 +/- 0.40 microM). Likewise, mesenteric arterioles from antisense ODN-treated rats revealed attenuation of myogenic constrictor responses to increases of transmural pressure. The decreased vascular reactivity and myogenic responses were reversible with the addition of 20-HETE. These data suggest that CYP4A1-derived 20-HETE facilitates myogenic constrictor responses in the mesenteric microcirculation and contributes to pressor mechanisms in SHR.

Adenoviral vector-mediated transfer of human heme oxygenase in rats decreases renal heme-dependent arachidonic acid epoxygenase activity.

Intravenous administration of an adenovirus human heme oxygenase (HO)-1 gene construct to rats resulted in functional expression of human HO-1 in brain, heart, lung, liver, and kidney. Because accurate assessment of human HO-1 mRNA in various tissues by Northern analysis is not sufficiently sensitive, we developed a method for quantifying human HO-1 mRNA copies with quantitative reverse transcription- polymerase chain reaction techniques; this allowed us to use the same primers for both the sample and internal standard. Administration of the adenovirus human HO-1 gene resulted in the detection of human HO-1 mRNA in various tissues with the highest levels seen in the kidney followed, in order, by lung > liver > brain > heart. Human HO-1 was detectable for up to 4 weeks in all tissues studied. Administration of adenovirus human HO-1 resulted in maximal increase of HO activity after 1 to 2 weeks in rats. The increase in HO activity due to gene transfer also was associated with a parallel decrease (approximately 25%) in cytochrome P-450 (CYP) content and in CYP-dependent arachidonic acid metabolism. In addition, we investigated the possibility that the human HO-1 gene altered the expression of the endogenous rat enzyme after administration of cobalt chloride s.c. Cobalt chloride administration resulted in increased HO activity in all tissues examined in rats transduced with the human HO-1 gene to the same degree as in nontransduced rats. The metal was a more potent inducer of renal HO activity than was the adenoviral-mediated human HO-1 vector. The increase in HO activity after adenoviral-mediated human HO-1 transfer was associated with a decrease in microsomal heme-CYP and CYP activity. The increase in HO-1 activity after adenovirus-mediated human HO-1 gene transfer may prove useful as a means of selectively increasing enzyme activity in a specific organ and regulating homeostasis by modulation of vasoactive molecules such as carbon monoxide and bilirubin and, in addition, providing a means of delivering the human HO-1 gene for experimental purposes.