Effectiveness of a 6-week online course in the Canadian Triage and Acuity Scale for emergency nurses.

INTRODUCTION: There is increasing interest in 5-level triage systems in emergency departments; however, the adoption of a new system places heavy training demands on ED department nurses and physicians. One emerging training option is online learning. The purpose of this study was to explore the effectiveness of an online course in the 5-level Canadian Triage and Acuity Scale (CTAS) on the clinical practice of the triage nurse. METHODS: Interviews were held with 23 emergency nurses from across Canada. A chart audit of triage codes from 367 charts from 6 hospitals was conducted. RESULTS: The most consistent finding was that the majority of RN staff enjoyed the online course and believed it had improved their triage practice. Nurses believed that their patient assessments were more thorough, accurate, and consistent throughout the department. Improved communication between staff and with patients and families was identified. Nurses reported using what they learned to improve triage assessment. Triage accuracy was high; the overall agreement between CTAS graduates and the chart auditor/expert within one CTAS level was 99.7%. Nurses also identified a number of organizational barriers to CTAS implementation after the course. DISCUSSION: The online format appears to be an effective, efficient, and convenient way to educate large numbers of ED staff in CTAS. Further research is needed regarding the use of multimedia and computer online chat options to further enhance the online learning experience for nurses.

Atypical presentation of acute myocardial infarction in 3 age groups.

OBJECTIVE: The purpose of this study was to compare the clinical manifestations of first-time acute myocardial infarction (AMI) in 3 age groups of men and women who presented to the emergency departments of 3 acute tertiary care hospitals. DESIGN: An exploratory, descriptive design was used, and there were 2 phases to the project. Phase 1 was a retrospective chart audit of a systematic random sample of patient charts, and phase 2 included a structured interview of a prospective random sample of emergency and intensive care unit nurses and physicians. The data were collected by using a chart audit tool and a semistructured interview, respectively. SETTING: The study took place at a western Canada university affiliated with acute tertiary care centres. SAMPLE: A systematic random sample of 153 (105 men and 48 women) patient charts were audited from the health records departments of 3 acute care hospitals. All of the patients had experienced a first-time AMI. In addition, a random sample of emergency/intensive care unit nurses (n = 60) and physicians (n = 18) was interviewed. RESULTS: The results indicate that a statistically significant number of the oldest (75 years or older) male patients present with atypical manifestations of AMI compared with the men in the younger age groups (P =.005). The same trend was not noted for female patients. The results of the study are limited with respect to the small number of women in each age category. Caution must therefore be exercised in generalizing the results to the target population of women with AMI. The atypical manifestations are described. The results of the interviews revealed that many clinicians do not look for different clinical manifestations when assessing older patients. CONCLUSIONS: It is essential that nurses and physicians accurately assess patients with AMI, especially patients in the older age groups who may be presenting atypically. It is also important that professional and nonprofessional public health education initiatives include information regarding both typical and atypical presentation of AMI, particularly in the older patient.

Expression of interleukin 9 in the lungs of transgenic mice causes airway inflammation, mast cell hyperplasia, and bronchial hyperresponsiveness.

Interleukin (IL)-9, a pleiotropic cytokine produced by the Th2 subset of T lymphocytes has been proposed as product of a candidate gene responsible for asthma. Its wide range of biological functions on many cell types involved in the allergic immune response suggests a potentially important role in the complex pathogenesis of asthma. To investigate the contributions of IL-9 to airway inflammation and airway hyperresponsiveness in vivo, we created transgenic mice in which expression of the murine IL-9 cDNA was regulated by the rat Clara cell 10 protein promoter. Lung selective expression of IL-9 caused massive airway inflammation with eosinophils and lymphocytes as predominant infiltrating cell types. A striking finding was the presence of increased numbers of mast cells within the airway epithelium of IL-9-expressing mice. Other impressive pathologic changes in the airways were epithelial cell hypertrophy associated with accumulation of mucus-like material within nonciliated cells and increased subepithelial deposition of collagen. Physiologic evaluation of IL-9-expressing mice demonstrated normal baseline airway resistance and markedly increased airway hyperresponsiveness to inhaled methacholine. These findings strongly support an important role for IL-9 in the pathogenesis of asthma.

Using scientific evidence to improve hospital library services: Southern Chapter/Medical Library Association journal usage study.

BACKGROUND: Journal usage studies, which are useful for budget management and for evaluating collection performance relative to library use, have generally described a single library or subject discipline. The Southern Chapter/Medical Library Association (SC/MLA) study has examined journal usage at the aggregate data level with the long-term goal of developing hospital library benchmarks for journal use. METHODS: Thirty-six SC/MLA hospital libraries, categorized for the study by size as small, medium, or large, reported current journal title use centrally for a one-year period following standardized data collection procedures. Institutional and aggregate data were analyzed for the average annual frequency of use, average costs per use and non-use, and average percent of non-used titles. Permutation F-type tests were used to measure difference among the three hospital groups. RESULTS: Averages were reported for each data set analysis. Statistical tests indicated no significant differences between the hospital groups, suggesting that benchmarks can be derived applying to all types of hospital libraries. The unanticipated lack of commonality among heavily used titles pointed to a need for uniquely tailored collections. CONCLUSION: Although the small sample size precluded definitive results, the study's findings constituted a baseline of data that can be compared against future studies.

Interleukin-4 alters epithelial cell differentiation and surfactant homeostasis in the postnatal mouse lung.

Interleukin-4 (IL-4) is a pleotrophic cytokine which is increased during lung injury and inflammation. Epithelial cell morphology and surfactant homeostasis were assessed in 4-52-wk-old transgenic mice in which IL-4 was expressed in the bronchial and bronchiolar epithelial cells under the control of the Clara cell secretory protein promoter (CCSP-IL-4 mice). IL-4 caused progressive pulmonary infiltration with macrophages, lymphocytes, neutrophils, and eosinophils. Epithelial cell hypertrophy and mucus cell metaplasia were observed in the lungs of CCSP-IL-4 mice at all ages. Airway epithelial cells contained increased neutral glycoproteins and expressed gastric mucin, normally absent in the bronchiolar epithelium of the mouse. Immunohistochemical and biochemical studies demonstrated increased surfactant proteins A and B in lung sections and lung homogenates of CCSP-IL-4 transgenic mice. Increased immunostaining for surfactant proprotein C was also detected in type II epithelial cells of the transgenic mice. In contrast, surfactant protein B and CCSP expression was decreased or was absent in hypertrophic epithelial cells lining the conducting airways of transgenic mice. Lung-specific increase in T-cell proliferative responses to mitogenic stimulation and antibody secretion were detected in CCSP-IL-4 mice. Differentiated characteristics of respiratory epithelial cells were dramatically influenced by the chronic production of IL-4 in the conducting airways. Alterations in lung morphology in the CCSP-IL-4 mice are similar to some of those induced by antigenic stimulation or associated with chronic airway inflammation.

A novel role for murine IL-4 in vivo: induction of MUC5AC gene expression and mucin hypersecretion.

Mucus hypersecretion and plugging of lower respiratory tract airways contributes to the morbidity and mortality associated with asthma. Interleukin (IL)-4 plays a putative role in some forms of asthma. Thus, transgenic mice that overexpress murine IL-4 selectively within the lung were used to study the effect of IL-4 on mucus glycoprotein gene expression and mucin release. Histologic examination of lung sections from IL-4 mice revealed that nonciliated epithelial cells from conducting airways were hypertrophic, due at least in part to the accumulation of mucus glycoprotein. The cytoplasm of these cells stained positively for glycoproteins using mucicarmine, alcian blue (AB), and periodic acid-Schiff (PAS). Ciliated cells were also enlarged but did not show any mucin-specific staining. Inclusion granules typically found in nonciliated (Clara) cells of control mice were absent in the IL-4 transgenic mice. Northern blot analysis of total RNA from lung tissue revealed that the expression of the MUC5AC, but not MUC2, mucin gene was distinctly upgraded in IL-4 transgenic mice compared to transgene-negative controls. In addition, a 5- to 10-fold increase in AB- and PAS-positive material was found in lavage fluid from IL-4 overexpressing mice compared to transgene-negative controls. Thus, the overexpression of IL-4 locally within the lung enhances mucus glycoprotein synthesis by altering gene expression, results in the accumulation of mucus glycoprotein in nonciliated epithelial cells, and induces the release of mucus into the airway lumen. We therefore hypothesize that the overproduction of mucus seen in some patients with asthma may be a direct result of the action of IL-4 within the inflamed lung.

Phenotypic and physiologic characterization of transgenic mice expressing interleukin 4 in the lung: lymphocytic and eosinophilic inflammation without airway hyperreactivity.

To investigate the contribution of interleukin-4 (IL-4) to airway inflammation in vivo and to explore directly its relationship to airway reactivity, we created transgenic mice in which the murine cDNA for IL-4 was regulated by the rat Clara cell 10 protein promoter. Expression was detected only in the lung and not in thymus, heart, liver, spleen, kidney, or uterus. The expression of IL-4 elicited hypertrophy of epithelial cells of the trachea, bronchi, and bronchioles. Hypertrophy is due, at least in part, to the accumulation of mucus glycoprotein. Histologic examination of parenchyma revealed multinucleated macrophages and occasional islands of cells consisting largely of eosinophils or lymphocytes. Analysis of lung lavage fluid revealed the presence of a leukocytic infiltrate consisting of lymphocytes, neutrophils and eosinophils. Mice expressing IL-4 had greater baseline airway resistance but did not demonstrate hyperreactivity to methacholine. Thus, the expression of IL-4 selectively within the lung elicits an inflammatory response characterized by epithelial cell hypertrophy, and the accumulation of macrophages, lymphocytes, eosinophils, and neutrophils without resulting in an alteration in airway reactivity to inhaled methacholine.

Respiratory syncytial virus induces interleukin-10 by human alveolar macrophages. Suppression of early cytokine production and implications for incomplete immunity.

Respiratory syncytial virus (RSV) causes repeated infections thought to be due to an ineffective immune response. We examined the hypothesis that incomplete immunity may result, in part, from RSV-infected alveolar macrophage production of IL-10 which can interfere with the production of immunoregulatory cytokines. We also assessed whether RSV induced the expression of the 2',5' oligoadenylate (2-5A)-dependent RNase L, an endoribonuclease involved in the antiviral activities of interferons. Human alveolar macrophages were exposed to medium (uninfected control), RSV, LPS, and RSV + LPS then were assessed for expression of the cytokines TNF-alpha, IL-1 beta, IL-8, IL-10, as well as 2-5A-dependent RNase L. LPS up-regulated the expression of protein and mRNA for all cytokines. RSV stimulated the protein levels of TNF-alpha, did not alter IL-1 beta, and decreased IL-8. RSV markedly stimulated protein expression of IL-10 and 2-5A-dependent RNase L. RSV had minor effects on the steady state mRNA levels of TNF-alpha, IL-1 beta, and IL-8, yet potently induced IL-10. Cells costimulated with RSV + LPS demonstrated reduced protein and mRNA levels of TNF-alpha, IL-1 beta, IL-8 but synergistically increased IL-10 levels compared to RSV- or LPS-activated cells. Kinetic analysis indicated that RSV induced a delayed and sustained increase in IL-10 transcripts. Furthermore, RSV-infected alveolar macrophage supernatants suppressed IL-1 beta and IL-8 production by LPS-stimulated alveolar macrophages as did recombinant IL-10. Anti-IL-10 neutralized these effects. These studies indicate that RSV is capable of suppressing production of early immunoregulatory cytokines through induction of IL-10 perhaps mediated by 2-5A-dependent RNase L (or other endoribonucleases) accounting for the ineffective immune response to this virus.

Implementing hospital library automation: the GaIN project. Georgia Interactive Network for Medical Information.

The GaIN (Georgia Interactive Network for Medical Information) Hospital Libraries' Local Automation Project was a one-year, grant-funded initiative to implement an integrated library system in three Georgia hospitals. The purpose of the project was to install the library systems, describe the steps in hospital library automation, and identify issues and barriers related to automation in small libraries. The participating hospitals included a small, a medium, and a large institution. The steps and time required for project implementation were documented in order to develop a decision checklist. Although library automation proved a desirable approach for improving collection accessibility, simplifying daily routines, and improving the library's image in the hospital, planners must be sure to consider equipment as well as software support, staffing for the conversion, and training of the library staff and end users.

Pathophysiology of the rheumatoid joint.

The precise cause of rheumatoid arthritis (RA) is, as yet, unknown. But with more sophisticated techniques in the fields of immunogenetics and molecular biology, there is increasing knowledge of the pathophysiology of the rheumatoid joint. Pathophysiologic knowledge should be part of the orthopaedic nurse's repertoire when dealing with the "whole" patient; therefore orthopaedic nurses who care for patients with rheumatoid disease should understand certain pathophysiologic concepts. This article reviews the pathophysiology of the rheumatoid joint and describes the changes that take place in the joint with specific reference to the cells of the immune system, the synovium, and articular cartilage.

Airway epithelial cell expression of interleukin-6 in transgenic mice. Uncoupling of airway inflammation and bronchial hyperreactivity.

We produced transgenic mice which overexpress human IL-6 in the airway epithelial cells. Transgenic mice develop a mononuclear cell infiltrate adjacent to large and mid-sized airways. Immunohistochemistry reveals these cells to be predominantly CD4+ cells, MHC class II+ cells, and B220+ cells. Transgenic mice and nontransgenic mice had similar baseline respiratory system resistance (0.47 +/- 0.06 vs 0.43 +/- 0.04 cmH2O/ml per s at 9 wk of age, P = NS and 0.45 +/- 0.07 vs 0.43 +/- 0.09 cmH2O/ml per s at 17 wk of age, P = NS). Transgenic mice, however, required a significantly higher log dose of methacholine to produce a 100% increase in respiratory system resistance as compared with non-transgenic littermates (1.34 +/- 0.24 vs 0.34 +/- 0.05 mg/ml, P < or = 0.01). We conclude that the expression of human IL-6 in the airways of transgenic mice results in a CD4+, MHC class II+, B220+ lymphocytic infiltrate surrounding large and mid-sized airways that does not alter basal respiratory resistance, but does diminish airway reactivity to methacholine. These findings demonstrate an uncoupling of IL-6-induced airway lymphocytic inflammation and airway hyperresponsiveness and suggest that some forms of airway inflammation may serve to restore altered airway physiology.

The effect of inhibition of leukotriene B4 release on lipopolysaccharide-induced production of neutrophil attractant/activation protein-1 (interleukin-8) by human alveolar macrophages.

Whereas we observed previously that concentrations of the lipoxygenase inhibitor nordihydroguaiaretic acid that inhibited leukotriene B4 release from lipopolysaccharide-stimulated human alveolar macrophages in vitro also inhibited subsequent interleukin-8 release, we hypothesized that leukotriene B4 release was required for the release of interleukin-8. Alveolar macrophages from normal nonsmoking volunteers were adhered to plastic and incubated with varying concentrations (25-250nM) of the 5-lipoxygenase activating protein inhibitor MK-886 prior to stimulation with lipopolysaccharide. MK-886 inhibited leukotriene B4 release in a concentration-dependent manner. The concentration of MK-886 that inhibited release by 50% was 53.3 +/- 23.1nM (mean +/- SD), n = 4. Interleukin-8 concentrations in 24hr supernatants were not inhibited by incubation of the cells with any concentration of MK-886, including those that inhibited leukotriene B4 release by > 95%. Thus, MK-886 is an effective inhibitor of human alveolar macrophage release of leukotriene B4, and the release of leukotriene B4 is not a prerequisite for alveolar macrophage release of interleukin-8.

Effects of in vitro amiodarone exposure on alveolar macrophage inflammatory mediator production.

Administration of amiodarone, although often lifesaving, is associated with pulmonary side effects. Patients with amiodarone pulmonary toxicity can present with either a chronic disorder that suggests pulmonary fibrosis or a more acute process. Mechanisms of acute pulmonary injury resulting from amiodarone are unclear. Previous studies have demonstrated that the drug is preferentially concentrated in alveolar macrophages. In the present study, the authors examined whether in vitro exposure to amiodarone resulted in alteration of rat alveolar macrophage superoxide, leukotriene B4, or fibronectin release. In addition, the authors assessed whether macrophages were ultrastructurally altered by in vitro amiodarone exposure. Twenty four hour exposure to therapeutic tissue concentrations of amiodarone resulted in enhancement of phorbol myristate acetate-stimulated macrophage superoxide release. In addition, 48 hours exposure to amiodarone caused a dose-dependent inhibition of spontaneous fibronectin release by macrophages. Macrophages exposed to 48 hours of 10 micrograms/ml amiodarone were ultrastructurally abnormal, containing lamellar inclusions and demonstrating a large degree of vacuolization. The authors concluded that alveolar macrophages are very sensitive to therapeutic tissue concentrations of amiodarone. Alteration of macrophage mediator release by amiodarone may be one mechanism for lung damage induced by the drug.

Anti-HIV-1 activity of 3'-azido-3'-deoxythymidine (AZT) in primary mononuclear phagocytes.

Conflicting data have been reported on ability of 3'-azido-3'-deoxythymidine (AZT) to protect mononuclear phagocytes from HIV-1 infection. We compared the antiviral potency of AZT in three types of primary human mononuclear phagocytes: peripheral blood monocytes, monocyte-derived macrophages (in vitro differentiated) and alveolar macrophages (in vivo differentiated). To establish highly-productive virus infection, purified cells (greater than 99%) from healthy donors were challenged with the macrophage-tropic HTLV-IIIBa-L strain at input multiplicities ranging from 0.05 to 20 TCID50 per cell. AZT (0.1 nM-10 microM) was added immediately after infection and either continued for the duration of the experiment or stopped 1-7 days after infection. The kinetics of HIV-1Ba-L replication were assessed by measuring p24 antigen production on days 4-28 post-infection. Continuous treatment with AZT reproducibly inhibited viral replication in a concentration-dependent manner in all three cell types. The IC90 of AZT was 0.04 microM in blood monocytes, 0.009 microM in monocyte-derived macrophages, and 0.0001 microM in alveolar macrophages (mean of 3-4 donors for each cell type). AZT was not cytotoxic at less than 10 microM as assessed by cell viability, cell protein, and interferon-gamma-activated H2O2-release. In experiments in which AZT treatment was stopped after infection, viral replication resumed after a lag of 7-14 days and increased exponentially toward control levels. This occurred despite initial inhibition of virus production to below the limit of p24 detection (approximately 50 pg/ml). These results indicate that AZT is a potent inhibitor of HIV-1 replication in primary mononuclear phagocytes regardless of the stage of cell differentiation, and that AZT is most active in tissue (alveolar) macrophages. AZT does not irreversibly block infection of mononuclear phagocytes, however, as viral replication resumes after removal of AZT.