The Role of Work Environment in Training Sustainment: A Meta-Analysis

OBJECTIVE: The purpose of this meta-analytic review is to examine the role of three work environment support variables (i.e., peer, supervisor, and organizational support) in training transfer and sustainment or long-term use of learned knowledge, skills, and attitudes (KSAs). BACKGROUND: Estimates demonstrate that little training is transferred to the job, wasting billions in organizational spending each year and resulting in significant loss to safety and individual and team performance. Prior research shows the importance of a supportive work environment to facilitating transfer; however, we know little of the relative importance of specific support variables. This study seeks to examine the unique roles of distinct support variables in training transfer. METHOD: A meta-analysis was conducted with multiple regressions to answer three primary research questions. RESULTS: All work environment support variables demonstrate moderate and positive correlations with transfer of training. Furthermore, multiple regressions demonstrate that each factor of the work environment explains unique variance as a predictor, with the model accounting for 32% of transfer and peer support accounting for most of R2. Motivation to transfer mediates the relationship between all three work environment support variables and transfer. Furthermore, three support variables are positively related to sustainment, with peer and supervisor support showing the strongest relationships. CONCLUSION: Findings illuminate the relative contribution of peer, supervisor, and organizational support to transfer and sustainment of training. As transfer continues to be an important yet understudied measure of the effectiveness of workplace training, these findings hold implications for both research and practice

Loss of <i>Atg12</i>, but not <i>Atg5</i>, in pro-opiomelanocortin neurons exacerbates diet-induced obesity

<div><p>The autophagy-related proteins ATG12 and ATG5 form a covalent complex essential for autophagy. Here, we demonstrate that ATG12 has distinct functions from ATG5 in pro-opiomelanocortin (POMC)-expressing neurons. Upon high-fat diet (HFD) consumption, mice lacking <i>Atg12</i> in POMC-positive neurons exhibit accelerated weight gain, adiposity, and glucose intolerance, which is associated with increased food intake, reduced ambulation, and decreased LEP/leptin sensitivity. Importantly, although genetic deletion of either <i>Atg12</i> or <i>Atg5</i> renders POMC neurons autophagy-deficient, mice lacking <i>Atg5</i> in POMC neurons do not exhibit these phenotypes. Hence, we propose nonautophagic functions for ATG12 in POMC neurons that counteract excessive weight gain in response to HFD consumption.</p></div

Decision Making On The Labor And Delivery Unit: An Investigation Of Influencing Factors

Objective The aim of this study was to describe the relationship between negative affect (NA), decision-making style, time stress, and decision quality in health care. Background Health care providers must often make swift, high-stakes decisions. Influencing factors of the decision-making process in this context have been understudied. Method Within a sample of labor and delivery nurses, physicians, and allied personnel, we used self-report measures to examine the impact of trait factors, including NA, decision-making style, and perceived time stress, on decision quality in a situational judgment test (Study 1). In Study 2, we observed the influence of state NA, state decision-making style, state time stress, and their relationship with decision quality on real clinical decisions. Results In Study 1, we found that trait NA significantly predicted avoidant decision-making style. Furthermore, those who were higher on trait time stress and trait avoidant decision-making style exhibited poorer decisions. In Study 2, we observed associations between state NA with state avoidant and analytical decision-making styles. We also observed that these decision-making styles, when considered in tandem with time stress, were influential in predicting clinical decision quality. Conclusion NA predicts some decision-making styles, and decision-making style can affect decision quality under time stress. This is particularly true for state factors. Application Individual differences, such as affect and decision-making style, should be considered during selection. Training to reduce time stress perceptions should be provided

Histologic and ultrastructural patterns in autophagic vacuolar myopathy.

<p><b>A and B.</b> Sharply defined, central areas of dark staining (“basophilic cores"; arrows) seen on H&E- (A) and trichrome- (B) stained sections of frozen material (subject #22). <b>C and D.</b> Rimmed vacuoles (arrowheads) seen on H&E- (C) and trichrome- (D) stained sections of frozen material (subject #23) <b>E–G.</b> Autophagic vacuoles with membrane-bound (E; subject #22) or “free-floating" (F; subject #27) cellular debris on electron microscopy. Curvilinear bodies in a hydroxychloroquine-treated subject (G; subject #23). Scale bars: A and B, 50 µM; C and D, 20 µM; E–G, 1 µm.</p

Quantification of LC3- and p62-positive fibers in FFPE material.

<p><b>A and B.</b> The percentage of LC3- (<b>A</b>) and p62-positive (<b>B</b>) fibers was significantly higher in autophagic myopathy group (squares) than in either normal control (circles) or drug-treated control group (diamonds). Each study subject is represented with a symbol; the lines indicate group means. ***, p<0.001; *, p<0.05. <b>C and D.</b> ROC analysis indicates that quantitative immunohistochemistry for either LC3 (C) or p62 (D) can successfully differentiate autophagic myopathy from control cases among drug-treated subjects.</p

Study subject characteristics.

# §<p>To minimize sampling error due to scant (^#) or patchy (^§) positivity, a total of 600 (rather than 200) fibers was counted.</p>*<p>Scattered basophilic cores were present.</p>**<p>Multiple rimmed vacuoles were present.</p><p>NA Not applicable.</p

Immunoblotting confirms the specificity of LC3 and p62 immunohistochemistry.

<p><b>A.</b> Wt (ATG7+/+) and autophagy-deficient (ATG7−/−) mouse embryonic fibroblasts (MEFs) were used as positive control. In wt MEFs, 8 h treatment with 30 µM chloroquine (CQ) increased the level of LC3-II and p62 proteins compared to the untreated control (UT); LC3-I was barely detectable in either sample. In autophagy-deficient MEFs, the level of LC3-I and p62 was high at baseline and did not change following CQ treatment; LC3-II was undetectable in both samples. GAPDH was used as a loading control. <b>B.</b> In subjects from the autophagic myopathy group, LC3-II and p62 protein level was increased relative to subjects from either normal or drug-treated control groups. LC3-I protein level was equally high in all samples, suggesting that this isoform is not detected by LC3 immunohistochemistry. Each lane contains sample from a different study subject, with subject ID numbers indicated on top. GAPDH was used as a loading control.</p

Cognition and Physiological Response

Complex tasks in large and error-prone environments require unobtrusive, unbiased and real-time measurement of cognitive variables to promote safety and to achieve optimal performance. Despite the prevalence of physiological measurement of cognitive constructs and cognitive performance, such as workload, little has been done to justify the inference of cognitive states from physiological measures. We develop a framework based on the extant literature to provide the groundwork for further validation of physiological measurement. Specifically, we leverage theoretically-grounded conditions of measurement to aid in investigating the logical sampling and construct validity for use of such metrics. Further meta-analytic investigation is warranted to validate the model and justify use of physiological measures

Role of genetic and electrolyte abnormalities in prolonged QTc interval and sudden cardiac death in end-stage renal disease patients

<div><p>Background</p><p>Patients with end-stage renal disease have very high mortality. In individuals on hemodialysis, cardiovascular deaths account for ~50% of all deaths in this population, mostly due to arrhythmia. To determine the causes of these arrhythmic deaths is essential in order to adopt preventive strategies. The main objective of this study was to investigate whether, the presence of QTc interval alterations, from electrolyte abnormalities or presence of rare genetic variants, could have a relationship with sudden arrhythmogenic deaths in end-stage renal disease patients.</p><p>Methods</p><p>We recorded the pre- and post-dialysis QTc interval in 111 patients undergoing hemodialysis. In 47 of them, we analyzed 24 SCD-related genes including the most prevalent genes associated with long QT syndrome using a custom resequencing panel.</p><p>Results</p><p>We found a positive although not significant association between the presence of long QTc and mortality in a subset of end-stage renal disease patients. In addition, in five patients with long QTc only after dialysis (21.7%) we detected rare potentially pathogenic genetic variants. Three out of these five carriers subsequently died suddenly.</p><p>Conclusions</p><p>Genetic background may be determinant in the risk of sudden cardiac death in these patients. We recommend evaluating the QTc interval before and after hemodialysis, and performing a genetic analysis of individuals with long QTc after hemodialysis.</p></div

The Smc5/6 Complex Restricts HBV when Localized to ND10 without Inducing an Innate Immune Response and Is Counteracted by the HBV X Protein Shortly after Infection

<div><p>The structural maintenance of chromosome 5/6 complex (Smc5/6) is a restriction factor that represses hepatitis B virus (HBV) transcription. HBV counters this restriction by expressing HBV X protein (HBx), which targets Smc5/6 for degradation. However, the mechanism by which Smc5/6 suppresses HBV transcription and how HBx is initially expressed is not known. In this study we characterized viral kinetics and the host response during HBV infection of primary human hepatocytes (PHH) to address these unresolved questions. We determined that Smc5/6 localizes with Nuclear Domain 10 (ND10) in PHH. Co-localization has functional implications since depletion of ND10 structural components alters the nuclear distribution of Smc6 and induces HBV gene expression in the absence of HBx. We also found that HBV infection and replication does not induce a prominent global host transcriptional response in PHH, either shortly after infection when Smc5/6 is present, or at later times post-infection when Smc5/6 has been degraded. Notably, HBV and an HBx-negative virus establish high level infection in PHH without inducing expression of interferon-stimulated genes or production of interferons or other cytokines. Our study also revealed that Smc5/6 is degraded in the majority of infected PHH by the time cccDNA transcription could be detected and that HBx RNA is present in cell culture-derived virus preparations as well as HBV patient plasma. Collectively, these data indicate that Smc5/6 is an intrinsic antiviral restriction factor that suppresses HBV transcription when localized to ND10 without inducing a detectable innate immune response. Our data also suggest that HBx protein may be initially expressed by delivery of extracellular HBx RNA into HBV-infected cells.</p></div