Leading among leaders: the dean in today's medical school.

The magnitude and pace of change in the health care environment demand that medical schools change. Leading in a time of great change is difficult, and it is ironic that just when stability in leadership is most needed, the average tenure of deans is dropping. Indeed, the path to leadership in academic medicine is strewn with inherent ironies, paradoxes, and idiosyncrasies. For example, few people who become leaders in academic medicine aspire to, plan for, or seek training for leadership, yet leadership skills are essential to meet today's complex institutional demands. Also, most medical school deans were once medical students, and were selected and trained to be assertive, independent physicians, not to collaborate. For faculty, the medical school environment traditionally values individual autonomy and rewards individual achievement, not behavior that supports a larger community interest. Yet today's deans must be skilled at collaborative behavior, since they must have a vision for their schools and find ways to offer direction to the faculty and others to realize that vision. The author offers ideas about leadership and its development, and stresses that good leaders must above all curtail their egos in order to do what is best for their institutions. What a dean does as an individual is not nearly as important as what a dean enables others to do. The author also provides a checklist of dean's characteristics and responsibilities to help deans-to-be understand the job and current deans to think about how to succeed and thrive. He concluded by reiterating that the culture of individual faculty success based on individual entrepreneurism is passé. To operate in the new collaborative culture, today's successful dean must meld persuasion with educational statesmanship, always informed by a vision of how the school can prosper and serve.

Sustaining the development of primary care in academic medicine. Working Group on Sustaining the Development of Academic Primary Care. Association of American Medical Colleges.

This article is the report of the Working Group on Sustaining the Development of Academic Primary Care, one of the six subgroups of the Advisory Panel on the Mission and Organization of Medical Schools (APMOMS) sponsored by the Association of American Medical Colleges (AAMC). To begin, the group draws a distinction between primary care and generalism. Primary care is a core domain of health care and, in the context of emerging integrated systems, will increasingly be a multidisciplinary shared function. Non-subspecialized physicians, or "generalists," are a key element in the provision of primary care, but do not act alone. Core competencies for primary care are central to the education of all physicians. Therefore, irrespective of workforce goals for generalist physicians, primary care should have a strong, central position in the medical school so that graduates can receive a sound general medical education and can be prepared for any specialty and for lifelong learning in an evolving health care system. For primary care to achieve that position, medical schools must integrate primary care into their missions, strategic plans, operation, organization, academic administrative structures, curriculum development, faculty development (both school- and community-based), resource development, alliances with appropriate clinical services networks, financial policy, and evaluation and educational monitoring systems. The group briefly describes the elements of those changes and also proposes ways that the AAMC and medical school leaders could promote the central role of primary care in medical schools.

Fulfilling the social contract between medical schools and the public.

To gain a better understanding of the effects of medical schools related to transformations in medical practice, science, and public expectations, the Association of American Medical Colleges (AAMC) established the Advisory Panel on the Mission and Organization of Medical Schools (APMOMS) in 1994. Recognizing the privileges academic medicine enjoys as well as the power of and the strain on its special relationship with the American public, APMOMS formed the Working Group on Fulfilling the Social Contract. That group focused on the question: What are the roles and responsibilities involved in the social contract between medical schools and various interested communities and constituencies? This article reports the working group's findings. The group describes the historical and philosophical reasons supporting the concept of a social contract and asserts that medical schools have individual and collective social contracts with various subsets of the public, referred to as "stakeholders." Obligations derive implicitly from the generous public funding and other benefits medical school receive. Schools' primary obligation is to improve the nation's health. This obligation is carried out most directly by educating the next generation of physicians and biomedical scientists in a manner that instills appropriate professional attitudes, values, and skills. Group members identified 27 core stakeholders (e.g., government, patients, local residents, etc.) and outlined the expectations those stakeholders have of medical schools and the expectations medical schools have of those stakeholders. The group conducted a survey to test how leaders at medical schools responded to the notion of a social contract, to gather data on school leaders' perceptions of what groups they considered their schools' most important stakeholders, and to determine how likely it was that the schools' and the stakeholders expectations of each other were being met. Responses from 69 deans suggested that the survey provoked thinking about the broad issue of the social contract and stakeholders. Leaders on the same campuses disagreed about what groups were the most important stakeholders. Similarly, the responses revealed a lack of national consensus about the most important stakeholders, although certain groups were consistently included in the responses. The group concludes that medical school leaders should examine their assumptions and perspectives about their institutions' stakeholders and consider the interests of the stakeholders in activities such as strategic planning, policymaking, and program development.

Phospholipase A activity associated with the growth of Rickettsia prowazekii in L929 cells.

Cultured L929 cells infected with Rickettsia prowazekii had a greatly increased rate of hydrolysis of fatty acid from the oleic acid-radiolabeled phospholipids of the host cell membranes. The incorporation of fatty acid into phospholipid in an infected cell was only moderately inhibited relative to a mock-infected cell. Thus, even if the release of fatty acid from phospholipid represented a steady state between hydrolysis and resynthesis of phospholipids, the increase in release of fatty acid was due principally to increased phospholipase A activity. The increased rate of hydrolysis did not occur only late in the rickettsial infection; this activity began early in infection and continued throughout the course of infection. The addition of tetracycline or chloramphenicol (antibiotics which inhibit rickettsial protein synthesis) to the infected cells caused a rapid and total abatement of this increased rate of phospholipid hydrolysis. In contrast, high concentrations of penicillin affected the morphology of the intracellular rickettsiae, but did not inhibit the phospholipase activity. This phospholipase A activity clearly damages the host cell during the rickettsial infection and may represent the activity by which R. prowazekii escapes from the host cell.

Acquisition of glucose by Rickettsia prowazekii through the nucleotide intermediate uridine 5'-diphosphoglucose.

The ability of Rickettsia prowazekii to transport potential sources of the glucose moiety of bacterial polysaccharides was determined. Transport was determined both by filtration assays and by centrifugation through nonaqueous layers. Uridine 5'-diphosphoglucose (UDPG) was transported, whereas glucose was not transported; the uptake of glucose phosphates, although greater than that for glucose, was markedly lower than the transport of UDPG. Furthermore, the activities of hexokinase and phosphoglucomutase, enzymes required for the metabolism of glucose and glucose 6-phosphate, were undetectable in rickettsial extracts. The uptake of UDPG had an extended time course and did not reach a plateau until 60 min. The maximum rate of uptake was 340 pmol/min per mg of protein, and the rate was half-maximal at a UDPG concentration of 220 microM. Measurement of true influx of UDPG was complicated by the low activity of this transport system and the metabolism of the UDPG. The uptake of labeled UDPG was markedly inhibited by a 10-fold excess of uridine monophosphate, uridine diphospho-N-acetylglucosamine, and uridine diphospho-N-acetylgalactosamine but not by a variety of other structurally related compounds.

Regulatory role of phosphate and other anions in transport of ADP and ATP by Rickettsia prowazekii.

ADP and ATP were transported in Rickettsia prowazekii by an obligate exchange system without prior hydrolysis. The uptake of ATP and ADP by the obligate exchange system in R. prowazekii was dependent upon the anionic composition of the medium. The rate of transport of ATP was about three times greater than that of ADP in the absence of anions, and the rates of transport of both were about doubled by a variety of anions. However, phosphate anions were able to stimulate greatly the uptake of ADP so that in the presence of these anions, the uptake of ATP and that of ADP were about equal. Millimolar concentrations of anions were required to elicit the stimulation of ADP and ATP transport. The ADP-dependent efflux of ADP and ATP was also greatly stimulated by phosphate anions. The stimulation of ADP and ATP transport required that the anions be present in the external medium, as preincubation of the rickettsiae with phosphate anions was neither necessary nor sufficient. The competitive inhibition of ATP uptake by ADP required phosphate anions, indicating that phosphate anions increased the affinity of ADP for the transport system. The role of phosphate in the regulation of ATP and ADP exchange and its significance are discussed.

Proline transport and metabolism in Rickettsia prowazekii.

Purified Rickettsia prowazekii cells were able to transport L-proline. The influx of this amino acid had a Kt of 14 microM and a Vmax of about 64 pmol/min per mg of protein. Proline could not be transported by heat-killed or metabolically poisoned rickettsiae or at 0 degrees C. The uptake of proline was linear for almost 2 h. More than 90% of the accumulated intracellular radioactivity was proline. This intracellular pool could not be chased out of the cell by excess non-radioactive proline and did not exit into a proline-free medium. These results indicate that intracellular proline was bound or that the cell had a very limited efflux component for proline transport. The influx of proline was specific: among various analogs tested, only 3,4-dehydro-D,L-proline was effective in inhibiting proline uptake. R. prowazekii cells were unable to utilize proline as an energy source to drive hemolysis, and no measurable evolution from the rickettsiae of CO2 derived from proline occurred. The activities of the enzymes pyrroline-5-carboxylate-reductase and pyrroline-5-carboxylate dehydrogenase were not detectable. These enzymes are important in anabolism and catabolism of proline, respectively, and, if present in R. prowazekii have activities less than 1% of those in Escherichia coli.

Cytoplasmic distinction of avirulent and virulent Rickettsia prowazekii: fusion of infected fibroblasts with macrophage-like cells.

L-929 cells with virulent or avirulent Rickettsia prowazekii growing in their cytoplasm were fused with cells of the macrophage-like cell line RAW264.7. Fusion occurred between the two cell types, producing heterokaryons containing R. prowazekii. Both the number of rickettsiae per infected heterokaryon and the percentage of heterokaryons infected with rickettsiae decreased in experiments with the avirulent strain compared to those with the virulent strain. These results indicate that the differential survival of the virulent strain in macrophages is some unknown function of the cytoplasm of the macrophage and that the distinction is not only at the phagolysosome level.

Effects of ethanol- and saline-base PGE1 on the canine cerebral circulation.

The effects of ethanol- and saline-base prostaglandin E1 (PGE1) on systemic arterial blood pressure ((ABP), cerebral blood flow (CBF), cerebral vascular resistance (CVR), and cerebrospinal fluid (CSF) pressure were determined in anesthetized dogs. Progressively greater carotid intra-arterial infusions of ethanol-base PGE1 moderately decreased systemic ABP and CVR while perfusion of the CSF system with PGE1 moderately increased ABP and CVR; CBF was unaffected by either route of administration and CSF pressure was constant except for a slight decrease at the lowest intraventricular perfusion rate. Similar infusions of PGE1 were administered in saline base solutions in another group of dogs. Carotid intra-arterial infusion decreased ABP and CBF moderately at the highest infusion rate and caused a transient increase in CSF pressure. Cerebrospinal fluid system perfusion increased ABP moderately but did not affect the other parameters. These data indicate that PGE1 does not have a significant effect on cerebral hemodynamics when infused via the CSF system, but may produce slight cerebral vasodilation when infused into the carotid arteries in an ethanol base. This vasodilation may be due to autoregulation.

Continuous infusion indicator dilution measurement of limb blood flow and vascular response to magnesium sulfate in normotensive and hypotensive men.

A constant infusion, indicator dilution technique for blood flow measurements in the forearm and hand of man was tested and validated in vitro and in vivo. This technique employs jet injection to improve mixing of indicator with arterial blood. The mixing characteristics of the jet injection system were studied in vitro in tubing simulating the brachial artery of man. In addition, actual blood flows in the isolated pump-perfused forelimbs of five dogs were compared with constant infusion, indicator dilution calculated flows. Measurements were also made of mixing and of blood flow in the forearm and hand of man. The technique was used to compare forearm and hand vascular responses with constant intrabrachial arterial infusions of magnesium sulfate in 13 normotensive and 13 essential hypertensive men. In vitro and in vivo the jet injection system significantly improved mixing of indicator with blood, as compared with mixing produced by standard infusion techniques, without causing hemolysis. In 30 measurements in isolated, perfused dog forelimbs the correlation coefficient between actual and calculated blood flow was 0.992. Resting limb vascular resistance in the hypertensive group was significantly higher than in the normotensive group. Limb vascular resistance in all 26 men decreased in response to intrabrachial-arterial infusion of 0.25% magnesium sulfate (8 ml/min). Rate of infusion of Mg(++) was 0.162 mEq/min. There was a significant positive linear correlation between level of initial limb vascular resistance and magnitude of response to magnesium sulfate. Vascular response data adjusted for this source of variation were similar in hypertensives and normotensives.The data suggest that this constant infusion, indicator dilution technique allows accurate calculation of total limb blood flow in man, provided that anomalous bifurcation of the brachial artery is not present. The data also suggest that the jet injection system improves mixing of substances with arterial blood. Thus, use of this system should especially aid reliability of studies of limb vascular responses to vasoactive agents infused into the brachial artery.