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Background Stress is highly prevalent in the U.S. society, especially in executives, and is a well-documented risk factor for a wide range of medical disorders. Knowledge of common sources of stress and predictive factors may help identify executives at risk of high stress and allow us to appropriately refer them for stress management treatment. Objective The primary aim of this study was to identify common sources of stress, predictors of high stress, and other correlates among executives. Methods This was a cross-sectional survey of executives who requested a stress management consult at our institution. We abstracted the data from a 14-item intake survey as well as from the patient interview. Results Of the 839 executives, 827 executives (98.6%) who were referred for individual stress management consults completed the stress-related questions of the survey; 51.3% of these executives reported having a high stress level. Study participants mostly struggled with the well-being measures of sleep, anxiety, energy level, and diet. The majority reported that their main stressor was work related (n = 540, 64.4%) followed by family related (n = 371, 44.2%), health related (n = 170, 20.3%), and work–life balance (n = 62, 7.4%). In unadjusted analysis, high stress was associated with younger age ( P = .006), lower quality-of-life scores ( P < .001), and less physical activity ( P < .001). In multivariable analyses, the strongest predictors for high stress level were younger age (odds ratios [OR] = 0.84, P = .045) and worse quality-of-life indicators such as anxiety (OR = 2.72, P < .001), diet (OR = 0.78, P = .02), and sleep (OR = 0.74, P < .003). Conclusion These findings suggest that executives with a high level of stress might be best helped through a multimodality stress management program. Our findings merit replication in larger studies and more definitive confirmation with prospective clinical trials.

Objectives: Persistent cognitive impairment after critical illness is an important healthcare problem forecasted to worsen in the near future. However, the epidemiology is insufficiently explored. We aimed to determine potentially modifiable risk factors during ICU hospitalization that play a significant role in developing persistent cognitive impairment. Design: An observational case-control study. Settings: Mayo Clinic ICUs between July 1, 2004, and November 20, 2015. Patients: We conducted a study nested in a large cohort of 98,227 adult critically ill patients. Using previously validated computable phenotypes for dementia and cognitive impairment, we determined the onset of cognitive impairment relative to ICU hospitalization and associated risk factors. The primary endpoint of the study was new and persistent cognitive impairment documented between 3 and 24 months after ICU discharge. Interventions: Unadjusted and adjusted analyses were performed to identify potentially modifiable risk factors during ICU hospitalization. Measurements and Main Results: Among 21,923 unique patients identified as cognitively impaired (22% of the entire ICU cohort), 2,428 (2.5%) developed incident new and persistent cognitive dysfunction after the index ICU admission. Compared with age- and sex-matched ICU controls (2,401 pairs), cases had higher chronic illness burden (Charlson Comorbidity Index, 6.2 vs 5.1; p < 0.01), and were more likely to have multiple ICU stays (22% vs 14%; p < 0.01). After adjustment for baseline differences, new and persistent cognitive dysfunction was associated with higher frequency of acute brain failure in the ICU, a higher exposure to severe hypotension, hypoxemia, hyperthermia, fluctuations in serum glucose, and treatment with quinolones or vancomycin. Association with sepsis observed in univariate analysis did not persist after adjustment. Conclusions: Cognitive dysfunction is highly prevalent in ICU patients. Incident new and persistent cognitive impairment is less common but important, potentially preventable problem after critical illness. Chronic comorbidities and number of ICU stays increase the risk of post-ICU cognitive dysfunction irrespective of age. Modifiable ICU exposures were identified as potential targets for future prevention trials.

AbstractObjectiveAcute myeloid leukemia (AML) can be subtyped based on recurrent cytogenetic and molecular genetic abnormalities with diagnostic and prognostic significance. Although cytogenetic characterization classically involves conventional chromosome and/or fluorescence in situ hybridization (FISH) assays, limitations of these techniques include poor resolution and the inability to precisely identify breakpoints.MethodWe evaluated whether an NGS‐based methodology that detects structural abnormalities and copy number changes using mate pair sequencing (MPseq) can enhance the diagnostic yield for patients with AML.ResultsUsing 68 known abnormal and 20 karyotypically normal AML samples, each recurrent primary AML‐specific abnormality previously identified in the abnormal samples was confirmed using MPseq. Importantly, in eight cases with abnormalities that could not be resolved by conventional cytogenetic studies, MPseq was utilized to molecularly define eight recurrent AML‐fusion events. In addition, MPseq uncovered two cryptic abnormalities that were missed by conventional cytogenetic studies. Thus, MPseq improved the diagnostic yield in the detection of AML‐specific structural rearrangements in 10/88 (11%) of cases analyzed.ConclusionUtilization of MPseq represents a precise, molecular‐based technique that can be used as an alternative to conventional cytogenetic studies for newly diagnosed AML patients with the potential to revolutionize the diagnosis of hematologic malignancies.