Background More than 1000 candidates applied for orthopaedic residency positions in 2014, and the competition is intense; approximately one-third of the candidates failed to secure a position in the match. However, the criteria used in the selection process often are subjective and studies have differed in terms of which criteria predict either objective measures or subjective ratings of resident performance by faculty. Questions/purposes Do preresidency selection factors serve as predictors of success in residency? Specifically, we asked which preresidency selection factors are associated or correlated with (1) objective measures of resident knowledge and performance; and (2) subjective ratings by faculty. Methods Charts of 60 orthopaedic residents from our institution were reviewed. Preresidency selection criteria examined included United States Medical Licensing Examination (USMLE) Step 1 and Step 2 scores, Medical College Admission Test (MCAT) scores, number of clinical clerkship honors, number of letters of recommendation, number of away rotations, Alpha Omega Alpha (AOA) honor medical society membership, fourthyear subinternship at our institution, and number of publications. Resident performance was assessed using objective measures including American Board of Orthopaedic Surgery (ABOS) Part I scores and Orthopaedics InTraining Exam (OITE) scores and subjective ratings by faculty including global evaluation scores and faculty rankings of residents. We tested associations between preresidency criteria and the subsequent objective and subjective metrics using linear correlation analysis and Mann-Whitney tests when appropriate. Results Objective measures of resident performance namely, ABOS Part I scores, had a moderate linear correlation with the USMLE Step 2 scores (r = 0.55, p \ 0.001) and number of clinical honors received in medical school (r = 0.45, p \ 0.001). OITE scores had a weak linear correlation with the number of clinical honors (r = 0.35, p = 0.009) and USMLE Step 2 scores (r = 0.29, p = 0.02). With regards to subjective outcomes, AOA membership was associated with higher scores on the global evaluation (p = 0.005). AOA membership also correlated with higher global evaluation scores (r = 0.60, p = 0.005) with the strongest correlation existing between AOA membership and the ''interpersonal and communication skills
BackgroundThe first changes associated with smoking are in the small airway epithelium (SAE). Given that smoking alters SAE gene expression, but only a fraction of smokers develop chronic obstructive pulmonary disease (COPD), we hypothesized that assessment of SAE genome-wide gene expression would permit biologic phenotyping of the smoking response, and that a subset of healthy smokers would have a “COPD-like” SAE transcriptome.Methodology/Principal FindingsSAE (10th–12th generation) was obtained via bronchoscopy of healthy nonsmokers, healthy smokers and COPD smokers and microarray analysis was used to identify differentially expressed genes. Individual responsiveness to smoking was quantified with an index representing the % of smoking-responsive genes abnormally expressed (ISAE), with healthy smokers grouped into “high” and “low” responders based on the proportion of smoking-responsive genes up- or down-regulated in each smoker. Smokers demonstrated significant variability in SAE transcriptome with ISAE ranging from 2.9 to 51.5%. While the SAE transcriptome of “low” responder healthy smokers differed from both “high” responders and smokers with COPD, the transcriptome of the “high” responder healthy smokers was indistinguishable from COPD smokers.Conclusion/SignificanceThe SAE transcriptome can be used to classify clinically healthy smokers into subgroups with lesser and greater responses to cigarette smoking, even though these subgroups are indistinguishable by clinical criteria. This identifies a group of smokers with a “COPD-like” SAE transcriptome.
BackgroundMicroarray technology provides a powerful tool for defining gene expression profiles of airway epithelium that lend insight into the pathogenesis of human airway disorders. The focus of this study was to establish rigorous quality control parameters to ensure that microarray assessment of the airway epithelium is not confounded by experimental artifact. Samples (total n = 223) of trachea, large and small airway epithelium were collected by fiberoptic bronchoscopy of 144 individuals and hybridized to Affymetrix microarrays. The pre- and post-chip quality control (QC) criteria established, included: (1) RNA quality, assessed by RNA Integrity Number (RIN) ≥ 7.0; (2) cRNA transcript integrity, assessed by signal intensity ratio of GAPDH 3' to 5' probe sets ≤ 3.0; and (3) the multi-chip normalization scaling factor ≤ 10.0.ResultsOf the 223 samples, all three criteria were assessed in 191; of these 184 (96.3%) passed all three criteria. For the remaining 32 samples, the RIN was not available, and only the other two criteria were used; of these 29 (90.6%) passed these two criteria. Correlation coefficients for pairwise comparisons of expression levels for 100 maintenance genes in which at least one array failed the QC criteria (average Pearson r = 0.90 ± 0.04) were significantly lower (p < 0.0001) than correlation coefficients for pairwise comparisons between arrays that passed the QC criteria (average Pearson r = 0.97 ± 0.01). Inter-array variability was significantly decreased (p < 0.0001) among samples passing the QC criteria compared with samples failing the QC criteria.ConclusionBased on the aberrant maintenance gene data generated from samples failing the established QC criteria, we propose that the QC criteria outlined in this study can accurately distinguish high quality from low quality data, and can be used to delete poor quality microarray samples before proceeding to higher-order biological analyses and interpretation.
Heguy A, Harvey BG, Leopold PL, Dolgalev I, Raman T, Crystal RG. Responses of the human airway epithelium transcriptome to in vivo injury. Physiol Genomics 29: 139 -148, 2007. First published December 12, 2006; doi:10.1152/physiolgenomics.00167.2006.-To identify genes participating in human airway epithelial repair, we used bronchoscopy and brushing to denude the airway epithelium of healthy individuals, sequentially sampled the same region 7 and 14 days later, and assessed gene expression by Affymetrix microarrays with TaqMan RT-PCR confirmation. Histologically, the injured area was completely covered by a partially redifferentiated epithelial layer after 7 days; by 14 days the airway epithelium was very similar to the uninjured state. At day 7 compared with resting epithelium, there were substantial differences in gene expression pattern, with a distinctive airway epithelial "repair transcriptome" of actively proliferating cells in the process of redifferentiation. The repair transcriptome at 7 days was dominated by cell cycle, signal transduction, metabolism and transport, and transcription genes. Interestingly, the majority of differentially expressed cell cycle genes belonged to the G2 and M phases, suggesting that the proliferating cells were relatively synchronized 1 wk following injury. At 14 days postinjury, the expression profile was similar to that of resting airway epithelium. These observations provide a baseline of the functional gene categories participating in the process of normal human airway epithelial repair that can be used in future studies of injury and repair in airway epithelial diseases. gene expression; lung; repair; cell cycle; microarray THE HUMAN TRACHEOBRONCHIAL TREE comprises 23 orders of dichotomous branching airways lined by a 0.2-m 2 continuous layer of pseudostratified epithelium comprising primarily basal cells, undifferentiated columnar cells, ciliated cells, and secretory cells (5,31,31). The airway epithelium plays a central role in maintaining the fluid and electrolyte balance in the epithelial lining fluid and in defending the lung from inhaled xenobiotics, particulates, gases, and pathogens (27,30,39). In the normal lung, the airway epithelium turns over slowly, but with injury, the epithelium rapidly regenerates, first to reestablish the continuity of the epithelial layer, and then to differentiate to reestablish the normal cell population (4,12,13,35). In all of the major human airway disorders, including chronic obstructive lung disease, asthma, and bronchogenic carcinoma, there is enhanced, albeit disordered, airway epithelial regeneration (19,27,40).Despite the importance of maintaining the airway epithelium in health and disease and the extensive data regarding the airway epithelium in culture and in experimental animals (11,21,22,26,32,37,48,49), little is known about the genetic program that mediates the regeneration of the human airway epithelium (32). To help define this genetic program, we have developed a strategy to force the epithelium to undergo regenera...
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