A longitudinal study of self-assessment accuracy

Although studies have examined medical students' ability to self-assess their performance, there are few longitudinal studies that document the stability of self-assessment accuracy over time. This study compares actual and estimated examination performance for three classes during their first 3 years of medical school. Methods  Students assessed their performance on classroom examinations and objective structured clinical examination (OSCE) stations. Each self-assessment was then contrasted with their actual performance using idiographic (within-subject) methods to define three measures of self-assessment accuracy: bias (arithmetic differences of actual and estimated scores), deviation (absolute differences of actual and estimated scores), and covariation (correlation of actual and estimated scores). These measures were computed for four intervals over the course of 3 years. Multivariate analyses of variance and correlational analyses were used to evaluate the stability of these measures. Results  Self-assessment accuracy measures were relatively stable over the first 2 years of medical school with a decease occurring in the third year. However, the correlational analyses indicated that the stability of self-assessment accuracy was comparable to the stability of actual performance over this same period. Conclusion  The apparent decline in accuracy in the third year may reflect the transition from familiar classroom-based examinations to the substantially different clinical examination tasks of the third year OSCE. However, the stability of self-assessment accuracy compares favorably with the stability of actual performance over this period. These results suggest that self-assessment accuracy is a relatively stable individual characteristic that may be influenced by task familiarity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75505/1/j.1365-2923.2003.01567.x.pd

Efficient adenovirus-mediated gene transfer into primary T cells and thymocytes in a new coxsackie/adenovirus receptor transgenic model

BACKGROUND: Gene transfer studies in primary T cells have suffered from the limitations of conventional viral transduction or transfection techniques. Replication-defective adenoviral vectors are an attractive alternative for gene delivery. However, naive lymphocytes are not readily susceptible to infection with adenoviruses due to insufficient expression of the coxsackie/adenovirus receptor. RESULTS: To render T cells susceptible to adenoviral gene transfer, we have developed three new murine transgenic lines in which expression of the human coxsackie/adenovirus receptor (hCAR) with a truncated cytoplasmic domain (hCARΔcyt) is limited to thymocytes and lymphocytes under direction of a human CD2 mini-gene. hCARΔcyt.CD2 transgenic mice were crossed with DO11.10 T cell receptor transgenic mice (DO11.hCARΔcyt) to allow developmental studies in a defined, clonal T cell population. Expression of hCARΔcyt enabled adenoviral transduction of resting primary CD4(+) T cells, differentiated effector T cells and thymocytes from DO11.hCARΔcyt with high efficiency. Expression of hCARΔcyt transgene did not perturb T cell development in these mice and adenoviral transduction of DO11.hCARΔcyt T cells did not alter their activation status, functional responses or differentiative potential. Adoptive transfer of the transduced T cells into normal recipients did not modify their physiologic localization. CONCLUSION: The DO11.hCARΔcyt transgenic model thus allows efficient gene transfer in primary T cell populations and will be valuable for novel studies of T cell activation and differentiation

Transcriptional networks specifying homeostatic and inflammatory programs of gene expression in human aortic endothelial cells.

Endothelial cells (ECs) are critical determinants of vascular homeostasis and inflammation, but transcriptional mechanisms specifying their identities and functional states remain poorly understood. Here, we report a genome-wide assessment of regulatory landscapes of primary human aortic endothelial cells (HAECs) under basal and activated conditions, enabling inference of transcription factor networks that direct homeostatic and pro-inflammatory programs. We demonstrate that 43% of detected enhancers are EC-specific and contain SNPs associated to cardiovascular disease and hypertension. We provide evidence that AP1, ETS, and GATA transcription factors play key roles in HAEC transcription by co-binding enhancers associated with EC-specific genes. We further demonstrate that exposure of HAECs to oxidized phospholipids or pro-inflammatory cytokines results in signal-specific alterations in enhancer landscapes and associate with coordinated binding of CEBPD, IRF1, and NFκB. Collectively, these findings identify cis-regulatory elements and corresponding trans-acting factors that contribute to EC identity and their specific responses to pro-inflammatory stimuli

Growth of Captive Juvenile Tripletail Lobotes surinamensis

Early-juvenile tripletail Lobotes surinamensis (n = 27; range 45–115 mm TL, 0 = 73.0 mm; range 3.2–34.7 g TW, 0 = 12.9 g) captured in pelagic Sargassum algae off coastal Mississippi in mid-July 1999 were reared in a recirculating seawater system for 210 days. Fish were maintained on a natural light-dark cycle and fed to satiation 3 times per day. Water temperature ranged from 25.2° to 29.0° C and salinity was 28.0‰. All fish were measured for length and weight on days 1, 60, 135 and 210 of the study. Between these dates, mean daily TL growth rates were 2.2 mm/day, 1.2 mm/day, and 1.0 mm/day, respectively, where as 0 daily TW growth rates were 2.9 g/day, 4.3 g/day, and 7.1 g/day. Over the entire study, 0 TL and TW growth rates were 1.4 mm/day and 4.9 g/day, respectively. There was a significant correlation between length and weight vs. date of measurement. At the end of the study, specimens ranged from 272–431 mm TL (0 = 359 mm) and from 443.9–2,380.0 g TW (0 = 1,012.5 g)

Measuring Accuracy of Automated Parsing and Categorization Tools and Processes in Digital Investigations

This work presents a method for the measurement of the accuracy of evidential artifact extraction and categorization tasks in digital forensic investigations. Instead of focusing on the measurement of accuracy and errors in the functions of digital forensic tools, this work proposes the application of information retrieval measurement techniques that allow the incorporation of errors introduced by tools and analysis processes. This method uses a `gold standard' that is the collection of evidential objects determined by a digital investigator from suspect data with an unknown ground truth. This work proposes that the accuracy of tools and investigation processes can be evaluated compared to the derived gold standard using common precision and recall values. Two example case studies are presented showing the measurement of the accuracy of automated analysis tools as compared to an in-depth analysis by an expert. It is shown that such measurement can allow investigators to determine changes in accuracy of their processes over time, and determine if such a change is caused by their tools or knowledge.Comment: 17 pages, 2 appendices, 1 figure, 5th International Conference on Digital Forensics and Cyber Crime; Digital Forensics and Cyber Crime, pp. 147-169, 201

T Helper 1 and T Helper 2 Cells Are Pathogenic in an Antigen-specific Model of Colitis

Dysregulated T cell responses to enteric bacteria have been implicated as a common mechanism underlying pathogenesis in rodent models of colitis. However, the bacterial species and T cell specificities that induce disease have been poorly defined. We have developed a model system in which target antigen, bacterial host, and corresponding T cell specificity are defined. OVA-specific T cells from DO11.RAG-2−/− TCR transgenic mice were transferred into RAG-2−/− recipients whose intestinal tracts were colonized with OVA-expressing or control Escherichia coli. Transfer of antigen-naive DO11.RAG-2−/− T cells into recipients colonized with OVA-E. coli resulted in enhanced intestinal recruitment and cell cycling of OVA-specific T cells; however, there was no development of disease. In contrast, transfer of polarized T helper (Th) 1 and Th2 populations resulted in severe wasting and colitis in recipients colonized with OVA-expressing but not control E. coli. The histopathologic features of disease induced by Th1 and Th2 transfers were distinct, but disease severity was comparable. Induction of disease by both Th1 and Th2 transfers was dependent on bacterially associated OVA. These results establish that a single bacterially associated antigen can drive the progression of colitis mediated by both Th1 and Th2 cells and provide a new model for understanding the immunoregulatory interactions between T cells responsive to gut floral antigens

Restricted Clonal Expression of IL-2 By Naive T Cells Reflects Differential Dynamic Interactions with Dendritic Cells

Limited frequencies of T cells express IL-2 in primary antigenic responses, despite activation marker expression and proliferation by most clonal members. To define the basis for restricted IL-2 expression, a videomicroscopic system and IL-2 reporter transgenic model were used to characterize dendritic cell (DC)–T cell interactions. T cells destined to produce IL-2 required prolonged interactions with DCs, whereas most T cells established only transient interactions with DCs and were activated, but did not express IL-2. Extended conjugation of T cells with DCs was not always sufficient to initiate IL-2 expression. Thus, there is intrinsic variability in clonal T cell populations that restricts IL-2 commitment, and prolonged engagement with mature DCs is necessary, but not sufficient, for IL-2 gene transcription