Tapping the power of information: an orientation for academic medical centers.

In September 1994 the Association of American Medical Colleges' (AAMC's) Advisory Panel on the Mission and Organization of Medical Schools (APMOMS) established a working group to address both the long-term and the immediate implications of the expanding capacity of and need for information technology (IT) within academic medical centers (i.e., medical schools and teaching hospitals). Over a two-year period, group members assessed the utilization of IT through surveys of current practices and interactions with acknowledge leaders in the field. They also had discussions with deans and other institutional leaders. The group developed the consensus that proper use of currently available IT is crucial to virtually every aspect of academic medicine's clinical, educational, and research missions. Moreover, current IT technology will be further enhanced by the powerful new applications that are nearing deployment. All group members agreed that IT must become a core competency of academic and medical centers (AMCs), the profession, and individual physicians and scientists to ensure the survival of AMCs in the current highly competitive environments. The authors outline their arguments for the development of strong information systems within AMCs and present basic characteristics of systems that show promise for successful implementation. The y review some of the major institutional obstacles that have hindered the planing and implementation of IT. They conclude with a list of practical institution strategies for success in planning and implementing IT systems, and suggestions for how the AAMC can help members achieve success in these activities.

Preserving medical schools' academic mission in a competitive marketplace.

To gain a better understanding of the effects on medical schools of transformations in medical practice, science, and public expectations, the AAMC in 1994 formed the Advisory Panel on the Mission and Organization of Medical Schools and appointed six working groups to address relevant issues. This article is a report of the findings of the Working Group on Preserving Medical Schools' Academic Mission in a Competitive Marketplace, which was charged with exploring how medical schools could acquire and/or preserve an adequate patient base for teaching, research, and income generation in a competitive marketplace. The other groups' reports will appear in future issues of Academic Medicine. To understand the diversity of approaches that schools have taken to achieve this goal and to preserve their missions, the group interviewed representatives of nine medical schools, selected to represent a cross section of U.S. medical schools. The interviews took place on four occasions between June 1995 and March 1996. The information and comments shared by participants helped the working group gain insight into the fundamental issues it had been charged to address, including those of new delivery structures, what value schools offer to delivery structures, how education and research can be incorporated and supported financially, possible new pressures on relationships between medical schools and teaching hospitals, changes in faculty physicians' employment relationships and terms, and the role of the medical school in graduate medical education. In collecting and analyzing the data, the working group focused on the distinction between protecting an institution's existing enterprise and preserving an institution's core mission. This article gives a detailed overview of the information and comments each school presented, organized under the appropriate question. The working group's conclusions and commentaries on the findings follow. An appendix presents more detailed summaries of the schools' presentations, organised as case studies. The picture that emerges is complex. The working group concluded that medical schools will take a variety of approaches to define and preserve their missions. Most, but not all, medical schools will be able to secure the patient bases necessary to fulfill their missions even in a competitive marketplace. However, the nature of many of the schools is likely to change, and it is not clear whether the core missions of education and research will continue at their present levels at all schools.

Preparing for health care reform and an LCME site visit: addressing the generalist-non-generalist imbalance.

PURPOSE: The purpose of the present study was to evaluate primary care outcomes for the Loma Linda University School of Medicine (LLUSM), using Association of American Medical Colleges (AAMC) data files. The two principal objectives were to estimate the percentages of LLUSM graduates who are practicing or will practice primary care medicine and to determine what information available on application to LLUSM is useful in predicting graduates' specialty choices (i.e., primary versus non-primary care). METHOD: In 1993-94 data were taken from several AAMC data files (available to all medical schools), including the Graduate Medical Education (GME) Tracking Census and the American Medical College Application Service (AMCAS) Applicant Master File. The second and fourth years after graduation were used as points of evaluation. Primary care (generalist) was defined as taking or having completed a residency in family practice, internal medicine, or pediatrics, and not having taken any fellowship training. RESULTS: Fourth year after graduation: 42.4% of the 1,064 LLUSM graduates (1983 to 1990) were training in or had completed residencies in family practice (19.8%), internal medicine (16.2%), or pediatrics (6.4%). Second year of GME: of the 1,365 LLUSM graduates (1983 to 1992), 49.3% were in the primary care pipeline (19.8% in family practice, 21.9% in internal medicine, and 7.6% in pediatrics). Two variables available on admission to medical school were associated with being in the primary care pipeline (second-year GME generalist): being a woman and being a member of a non-underrepresented minority. One variable was associated with being in the non-primary care pipeline: having a rural county code. Undergraduate grades and Medical College Admission Test scores were not good predictors. CONCLUSION: The AAMC data files, available to all medical schools, are useful for estimating and evaluating primary care outcomes.

Comparison of the evolving histopathology of early and late cutaneous and asthmatic responses in rabbits after a single antigen challenge.

Histopathologic changes during the immediate cutaneous response (ICR) and late cutaneous response (LCR) to antigen challenge in allergic humans include dermal edema in the ICR (15 to 30 minutes) followed by increasing cellular infiltration in the LCR (6 hours and more). No description of the evolving histopathologic changes that occur during an immediate asthmatic response (IAR) followed by a late asthmatic response (LAR) exists in either clinical studies or animal models. We examined cutaneous and pulmonary histopathology at 1/2, 6, 24, and 48 hours as well as 7 days after simultaneous intradermal and aerosol antigen challenge of rabbits immunize with Alternaria tenuis extract. Nonimmunized rabbits challenged with Alternaria tenuis extract and immunized rabbits challenged with normal saline served as controls. Immediate wheal and flare responses followed by a LCR were seen in immunized but not control animals. Pulmonary function tests documented immediate and LAR in immunized but not control animals. Thirty minutes after antigen challenge of sensitized animals (ICR and IAR), both dermal sites and large airway submucosal sites had interstitial edema and vessel dilatation while small airways were essentially normal. At 6 hours after challenge, the dermal and large airway submucosal sites of immune animals (LCR and LAR) demonstrated a moderate mixed leukocyte infiltrate as well as residual edema. Additionally, bronchioles and pulmonary vessel adventitia from these responding animals had an intense and widespread leukocyte infiltration. At 24 and 48 hours, immune challenged animals but not controls had a marked mixed cellular infiltrate near skin vessels and near the bronchioles and pulmonary vessels with little or no residual interstitial edema. At 7 days, three of four animals showed resolution of the inflammation while the fourth showed minimal residual changes. Morphometric analysis of airway inflammation substantiated these qualitative observations and demonstrated that the granulocytes around airways of immune rabbits were a mixture of neutrophils and eosinophils at 6 hours, but were predominantly eosinophils at 48 hours. Immunofluorescent studies of skin and lung tissue did not demonstrate any granular or linear deposition of immunoglobulin or complement at the sites of inflammation, however, fibrin deposition was noted in the skin and lungs of immune rabbits. These observations show that immunized rabbits challenged with antigen develop cutaneous and pulmonary inflammation.(ABSTRACT TRUNCATED AT 400 WORDS)

The inflammatory reaction in the airways in an animal model of the late asthmatic response.

The late asthmatic response is defined as airway obstruction that occurs hours after antigen exposure in some atopic asthmatics. The importance of this reaction is that the airway obstruction may be severe, prolonged, and difficult to control unless corticosteroids are employed. In addition, this response may lead to an increase in airway reactivity. To investigate the immunopathogenesis of this disorder, an animal model in rabbits was developed. In this model, antigen-specific IgE was associated with the late asthmatic response and antigen-specific IgG was associated with blunting of the reaction. Antigen challenge of immune rabbits led to edema within the large airways shortly after antigen exposure, with infiltration of inflammatory cells (neutrophils and eosinophils) into the large and small airways during the late response. The infiltrates became more mononuclear with time and resolved over 10 days. As in humans, the late response was associated with an increase in airway reactivity and correlated temporally with infiltration of the airways with neutrophils and eosinophils. The contribution of granulocytic cells to the airway responses to antigen was studied by granulocyte depletion, which prevented both the late response and the heightened airway reactivity. In addition, transfusion of a neutrophil-rich population of white cells into granulocytopenic immune rabbits restored both responses. Thus, in this animal model, the antigen-induced late asthmatic response and subsequent increase in airway reactivity were dependent on the presence of granulocytes at the time of exposure to antigen.

Increases in airway reactivity to histamine and inflammatory cells in bronchoalveolar lavage after the late asthmatic response in an animal model.

An increase in airway reactivity after the late asthmatic response (LAR) has been noted in humans. Although these alterations in reactivity have been proposed to be associated with inflammation, no clinical study of the LAR has shown both increased airway reactivity and evidence of pulmonary inflammation. Employing an animal model of the LAR in rabbits developed in our laboratory (Am Rev Respir Dis 1982; 126:493-498), we examined changes in airway reactivity and pulmonary inflammation in rabbits having a late asthmatic response. Two groups of rabbits were studied: a control group (n = 10) received nonimmune serum, and a sensitized group (n = 10) received serum containing homocytotropic antibody (IgE) to ragweed extract (RWE) from rabbits previously immunized from birth with ragweed. Airway reactivity to histamine and the evaluation of different cell types in bronchoalveolar lavage fluid were determined 3 days before and 3 days after bronchial challenge with RWE in all rabbits. No control rabbit developed a LAR, and no significant changes occurred in this group's airway reactivity or cells in lavage fluid after bronchial challenge with RWE. In contrast, all sensitized rabbits developed a LAR, and airway reactivity for this group was markedly increased 3 days later. In addition, the total number of cells including both polymorphonuclear and mononuclear cells in lavage fluid increased significantly 3 days after the LAR. Ten days after the LAR in the sensitized group (n = 8), as airway reactivity returned towards baseline, so did the cells in lavage. We conclude that increased airway reactivity to histamine is temporally associated with pulmonary inflammation as defined by cells in lavage after the LAR in this model.

Modulation of the late asthmatic response by antigen-specific immunoglobulin G in an animal model.

The late asthmatic response (LAR) occurs 4 to 12 h after antigenic challenge and has been related to the severity of asthma. In addition, improvement of asthmatic symptoms after immunotherapy has also been related to loss of the LAR. Because the LAR seems to be a critical component of asthma, we employed an animal model of the LAR to study its immunopathogenesis, concentrating on the role of antigen-specific rabbit homocytotropic (IgE) and heterocytotropic (IgG) antibodies to Alternaria tenuis. Serum samples from rabbits previously immunized with Alternaria extract were infused into age-matched previously nonimmunized recipients. Groups of recipients were categorized according to the immune status of the transfused serum: E-only, E/G, subdivided into E/low G (1:256 to 1:512) and E/high G 1:2,048), G (serum heat-treated to minimize IgE), and Control (transfused with serum from nonimmunized rabbits). Subsequently, pulmonary function was measured before and for 6 h after challenge with aerosolized Alternaria tenuis by recording pulmonary resistance, functional residual capacity by helium dilution, specific conductance, and dynamic compliance. The E-only recipients showed an immediate asthmatic response followed by a marked LAR comparable in magnitude to actively immunized animals. The E/G recipients showed blunting of the LAR in a dose-dependent fashion, with increasing titers of IgG antibody. The G recipients showed no immediate or late responses. Immunofluorescent studies in selected animals from each group failed to show any granular deposition of immunoglobulin or C3 in either the airways or blood vessels of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

An animal model of late pulmonary responses to Alternaria challenge.

The pathogenesis of the late asthmatic response to allergen inhalation is unknown; IgE as well as IgE- and IgG-dependent mechanisms have been proposed. This study was undertaken to determine whether rabbits immunized to produce only IgE to Alternaria tenius would develop immediate and late phase pulmonary responses to Alternaria aerosol challenge, and to compare this response in "IgE only" rabbits with the response in rabbits producing multiple antibody isotypes to the allergen. Neonatal rabbits immunized with Alternaria tenius extract produced only IgE to that allergen, whereas rabbits first immunized at 7 days of age made multiple antibody isotypes. After aerosol challenge, the rabbits with only IgE antibody to the Alternaria developed biphasic change in lung function, as assessed by changes in pulmonary resistance and dynamic compliance, whereas rabbits with anti-Alternaria IgG as well as IgE had blunted biphasic pulmonary responses. Intravenously administered isoproterenol did not reverse the late phase response. Transfusion with serum containing anti-Alternaria IgG into "IgE only" rabbits reduced both the early and late phase changes in pulmonary mechanics. Transfusion of plasma containing anti-Alternaria IgE into nonimmunized control rabbits produced, upon challenge, both early and late phase responses in pulmonary mechanics, which were lost in retesting 4 wk later. We conclude that in this system IgE-allergen interaction can result in both the immediate and late pulmonary responses, that the presence of IgG results in blunting rather than in enhancing of this responsiveness, and that the response can be seen in the absence of cellular immune mechanisms.