Developing resources to teach and assess the core competencies: a collaborative approach.

Graduate medical education programs face new challenges as they seek to comply with the mandate from the Accreditation Council on Graduate Medical Education to demonstrate that they are teaching and assessing residents on the six core competencies. The authors describe a project designed as a collaborative venture between the American Academy of Allergy, Asthma, and Immunology (AAAAI) and the Center for Educational Outcomes at Dartmouth College (CEdO) to provide residency programs in allergy/immunology with resources for teaching and assessing the core competencies. The goal was to create a set of learning and assessment resources that maximized the content knowledge expertise provided by the AAAAI and the learning expertise provided by CEdO. A highly interactive, iterative process was used to create a set of Web-based modules. Bilateral communication, buy-in, and active involvement in the process were seen as crucial to the development of resources and their successful implementation. Approximately 18 months after the modules were made available to training program directors, 80% of the directors surveyed were aware of and had accessed the modules. The joint creation process used in this project, designed to be generally applicable across specialties, reveals how the burden of meeting new requirements can be decreased when experts in content knowledge and experts in learning collaborate.     

Role of Adherence in the Pathogenesis of Neonatal Group B Streptococcal Infection

The ability of group B streptococci to attach to buccal epithelial cells from adult volunteers, healthy neonates, and infants with invasive group B streptococcal infection was assessed by using (3)H-labeled bacteria incubated at a bacteria-to-cells ratio of 1,000:1. Type III group B streptococcal clinical isolates adhered significantly better to the epithelial cells of healthy neonates than to those of adults (mean bacteria per cell of 31 versus 7, respectively; P < 0.005). In contrast, no statistically significant differences in adherence of type Ia or type II strains to cells of neonates and adults were noted. The adherence of strains isolated from 15 infants with invasive group B streptococcal infection was significantly greater to the cells of infected infants than to those of age-matched controls (mean bacteria per cell of 39 versus 18, respectively; P < 0.005). In contrast, no significant difference was noted in the adherence of a usually adherent type Ia strain and a nonadherent type III strain to the cells of infected infants compared with control infants. These results indicate that the serotype of group B streptococci with the greatest virulence for neonates (type III) adheres better to neonatal than to adult epithelial cells. Infants who develop invasive infection may have an increased number of epithelial cell surface receptor sites for attachment of group B streptococci, the bacteria may elaborate products which unmask receptor sites, or both.     

Characterization of the dominant autoreactive T-cell epitope in spontaneous autoimmune haemolytic anaemia of the NZB mouse

NZB mice spontaneously develop autoimmune haemolytic anaemia (AIHA) due to a T helper-dependent autoantibody response against the erythrocyte anion channel protein, Band 3. Here, we characterize the recognition of the Band 3 sequence 861-874, which carries the dominant, I-E(d)-restricted T cell epitope. The ability of N and C-terminal truncated versions of peptide 861-874 to elicit NZB splenic T-cell proliferation indicated that the core epitope spans residues 862-870. Next, a set of alanine substitution analogues was tested to determine which residues functioned either as MHC anchor or TCR contact residues. A combination of proliferation and MHC:peptide binding assays identified residues 862(L), 864(V), 865(L), and 869(K) as I-E(d) anchor residues, and 868(V) as the only TCR contact residue. The ability of the wild-type sequence 861-874 to compete with a high affinity reference peptide for binding to I-E(d) indicates that the escape of pathogenic NZB T cells from purging of the autoreactive repertoire cannot be attributed to ineffective presentation of peptide 861-874 by its restricting element. It will now be possible to design altered peptide ligands of Band 3 861-874, in order to further dissect the mechanisms responsible for the maintenance and loss of T cell tolerance to RBC autoantigens, and to modulate the immune response in AIHA.     

Malignant ameloblastoma,spindle cell variant

In this report, we document the histologic and clinical features of a previously undefined spindle cell variant of ameloblastoma that eventually behaved in a malignant fashion during a protracted course. The predominant histologic pattern was a well-differentiated, cellular, spindled epithelial proliferation arising in the maxilla of a 14-year-old African American girl. Over 19 years, the patient experienced numerous local recurrences, metastases to distant bones after 15 years, and finally bulky local recurrence with intracranial extension resulting in death. This ameloblastic malignancy histologically simulates a low-grade true sarcoma or an ameloblastic sarcoma, but differs in that the extensive spindle cell proliferation is epithelial, characterized by strong cytokeratin immunoreactivity and negative vimentin staining.     

Application of simple anthropometry in the assessment of health risk: implications for the Canadian Physical Activity, Fitness and Lifestyle Appraisal.

Incremental improvements in our knowledge of the associations between human body composition and disease have been facilitated by advances in research technology. Magnetic resonance imaging and computerized tomography are among the technological advances that have helped unravel the mechanisms that link body composition and disease. However, because the use of these methods in large-scale studies and field settings is impractical, the potential relationships between body composition and health risk rely on the use of anthropometric tools. Indeed, the application of simple anthropometry to identify relationships between body composition and health risk in clinical practice is no less valuable than the use of advanced technologies to gain insight into the mechanistic links between body composition and disease in the laboratory. Accordingly, the purpose of this review is to summarize current knowledge regarding the ability of anthropometry to predict health risk and to act as surrogate measures of total and abdominal fat distribution. Because the ultimate objective is to make recommendations for revision to the Healthy Body Composition section of the Canadian Physical Activity, Fitness and Lifestyle Appraisal (CPAFLA) manual, we focus on those anthropometric methods specific to CPAFLA. Consistent with this objective, when necessary we present original data to reinforce important concepts not suitably addressed in the literature.     

Peak Identification in Visual Evoked Potentials

Waveform patterns evoked by 4 intensities of flash in normal subjects were studied in relation to intersubject variability. Time-frequency distribution curves of all peaks occurring between 11 and 280 msec after flash onset and meeting minimal criteria were obtained from 46 males. These distributions closely corresponded to similar data reported by others for single intensity stimulation. An algorithm was developed which identified in 67 to 100% of instances a single “peak event’ within the time ranges of each of 6 peak distributions. Many peak events appeared and disappeared within the 4 intensity sets of individuals. Latencies were obtained for these peak events. Application of the algorithm to a replicate sample of 29 Ss, which included 8 females, indicated generalizability. Test-retest data on 15 Ss showed its reliability. The data suggest that methodology significantly contributes to the variability of peak identification among subjects. This may be reduced by employing multiple intensities of stimulation.     

Dipeptidyl peptidase 9 sets a threshold for CARD8 inflammasome formation by sequestering its active C-terminal fragment

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