The image candidates portray in the interview, via appearance, impression management, and verbal and nonverbal behavior, has been hypothesized to influence interviewer ratings. Through the lenses of social influence and interdependence theories, this meta-analysis investigated (a) the magnitude of the relationship between these 3 self-presentation tactics and interviewer ratings, (b) whether these tactics also are correlated with later job performance, and (c) whether important theoretical moderators (e.g., the level of interview structure, the rating source, the use of field or experimental designs) affect these relationships. Results reveal that what you see in the interview may not be what you get on the job and that the unstructured interview is particularly impacted by these self-presentation tactics. Additionally and surprisingly, moderator analyses of these relationships found that the type of research design (experimental vs. field) does not moderate these findings.

BACKGROUND There is debate about the value of assessing levels of C-reactive protein (CRP) and other biomarkers of inflammation for the prediction of first cardiovascular events. METHODS We analyzed data from 52 prospective studies that included 246,669 participants without a history of cardiovascular disease to investigate the value of adding CRP or fibrinogen levels to conventional risk factors for the prediction of cardiovascular risk. We calculated measures of discrimination and reclassification during follow-up and modeled the clinical implications of initiation of statin therapy after the assessment of CRP or fibrinogen. RESULTS The addition of information on high-density lipoprotein cholesterol to a prognostic model for cardiovascular disease that included age, sex, smoking status, blood pressure, history of diabetes, and total cholesterol level increased the C-index, a measure of risk discrimination, by 0.0050. The further addition to this model of information on CRP or fibrinogen increased the C-index by 0.0039 and 0.0027, respectively (P<0.001), and yielded a net reclassification improvement of 1.52% and 0.83%, respectively, for the predicted 10-year risk categories of “low” (<10%), “intermediate” (10% to <20%), and “high” (≥20%) (P<0.02 for both comparisons). We estimated that among 100,000 adults 40 years of age or older, 15,025 persons would initially be classified as being at intermediate risk for a cardiovascular event if conventional risk factors alone were used to calculate risk. Assuming that statin therapy would be initiated in accordance with Adult Treatment Panel III guidelines (i.e., for persons with a predicted risk of ≥20% and for those with certain other risk factors, such as diabetes, irrespective of their 10-year predicted risk), additional targeted assessment of CRP or fibrinogen levels in the 13,199 remaining participants at intermediate risk could help prevent approximately 30 additional cardiovascular events over the course of 10 years. CONCLUSIONS In a study of people without known cardiovascular disease, we estimated that under current treatment guidelines, assessment of the CRP or fibrinogen level in people at intermediate risk for a cardiovascular event could help prevent one additional event over a period of 10 years for every 400 to 500 people screened. (Funded by the British Heart Foundation and others.)

SummaryBackgroundPersistent inflammation has been proposed to contribute to various stages in the pathogenesis of cardiovascular disease. Interleukin-6 receptor (IL6R) signalling propagates downstream inflammation cascades. To assess whether this pathway is causally relevant to coronary heart disease, we studied a functional genetic variant known to affect IL6R signalling.MethodsIn a collaborative meta-analysis, we studied Asp358Ala (rs2228145) in IL6R in relation to a panel of conventional risk factors and inflammation biomarkers in 125 222 participants. We also compared the frequency of Asp358Ala in 51 441 patients with coronary heart disease and in 136 226 controls. To gain insight into possible mechanisms, we assessed Asp358Ala in relation to localised gene expression and to postlipopolysaccharide stimulation of interleukin 6.FindingsThe minor allele frequency of Asp358Ala was 39%. Asp358Ala was not associated with lipid concentrations, blood pressure, adiposity, dysglycaemia, or smoking (p value for association per minor allele ≥0·04 for each). By contrast, for every copy of 358Ala inherited, mean concentration of IL6R increased by 34·3% (95% CI 30·4–38·2) and of interleukin 6 by 14·6% (10·7–18·4), and mean concentration of C-reactive protein was reduced by 7·5% (5·9–9·1) and of fibrinogen by 1·0% (0·7–1·3). For every copy of 358Ala inherited, risk of coronary heart disease was reduced by 3·4% (1·8–5·0). Asp358Ala was not related to IL6R mRNA levels or interleukin-6 production in monocytes.InterpretationLarge-scale human genetic and biomarker data are consistent with a causal association between IL6R-related pathways and coronary heart disease.FundingBritish Heart Foundation; UK Medical Research Council; UK National Institute of Health Research, Cambridge Biomedical Research Centre; BUPA Foundation.

Objective To estimate the association of posttraumatic stress disorder (PTSD) with risk for incident coronary heart disease (CHD) Design Systematic review and meta-analysis Data sources Ovid MEDLINE, PsycINFO, Scopus, Cochrane Library, PILOTS database, PubMed Related Articles, and a manual search of reference lists (1948-present) Study selection All studies that assessed PTSD in participants initially free of CHD and subsequently assessed CHD/cardiac-specific mortality were included. Data extraction Two investigators independently extracted estimates of the association of PTSD to CHD, as well as study characteristics. Odds ratios were converted to hazard ratios (HR), and a random-effects model was used to pool results. A secondary analysis including only studies that reported estimates adjusted for depression was conducted. Results Six studies met our inclusion criteria (N= 402,274); 5 of these included depression as a covariate. The pooled HR for the magnitude of the relationship between PTSD and CHD was 1.55 (95% CI, 1.34–1.79) before adjustment for depression. The pooled HR estimate for the 5 depression-adjusted estimates (N= 362,950) was 1.27 (95% CI, 1.08–1.49). Conclusion PTSD is independently associated with increased risk for incident CHD, even after adjusting for depression and other covariates. PTSD is common in both military veterans and civilian trauma survivors, and these results suggest that it may be a modifiable risk factor for CHD. Future research should identify mechanisms of this association and determine whether PTSD treatment offsets CHD risk.

Importance-There are concerns about the current quality of undergraduate medical education (UME) and its effect on students' well-being.Objective-This systematic review was designed to identify best practices for UME learning environment interventions that are associated with improved emotional well-being of students.Data Sources-Learning environment interventions were identified by searching the biomedical electronic databases Ovid MEDLINE, EMBASE, the Cochrane Library, and the ERIC database from the database inception dates to October 2016. Studies examined any intervention designed to promote medical students' emotional well-being in the setting of a US academic medical school, with an outcome defined as students' reports of well-being as assessed by surveys, semistructured interviews, or other quantitative methods.Data Extraction and Synthesis-Two investigators independently reviewed abstracts and full-text articles. Data were extracted into tables to summarize results. Study quality was assessed by the Medical Education Research Study Quality Instrument (MERQSI), which has a possible range of 5-18; higher scores indicate higher design and methods quality, and a score of ≥ 14 indicates a high-quality study.Findings-Twenty-eight articles including at least 8224 participants met eligibility criteria. Study designs included single-group cross-sectional or post-test only (n=10), single-group pre-/ post-test (n=2), nonrandomized two-group (n=13), and randomized clinical trial (n=3); 93% were