A Quality Improvement Curriculum for Psychiatry Residents.

Introduction: Quality improvement (QI) is an increasingly important aspect of health care and residency education. There is relatively little research describing QI curricula for residents in psychiatry. Although QI curricula have been published in MedEdPORTAL, the current resource represents the first such curriculum specific to psychiatry residents. This resource aims to present a QI curriculum for psychiatry residents. Methods: The University of Wisconsin psychiatry residency program implemented a QI curriculum for our PGY 3 psychiatry residents in 2010. The initial version of the curriculum has undergone marked changes over the ensuing years, reflecting feedback received from learners and faculty instructors, as well as ongoing review of the literature, to ascertain best practices in this area of medical education. Steps taken have included faculty training, development of evaluation forms, and implementation of elements to increase accountability for successful, sustainable project development. Results: During the 8 completed years of this curriculum, 77 PGY 3 psychiatry residents have completed it. The Quality Improvement Knowledge Application Tool adapted for psychiatry was completed by PGY 3 residents in advance of and upon completion of the curriculum for the first 2 years of the curriculum; results demonstrated a significant improvement in scores as a measurement of QI knowledge and skills. Thirty-one of 32 resident teams (97%) have implemented a QI project. Discussion: Our QI curriculum for PGY 3 psychiatry residents has been successful in equipping residents with QI knowledge and having them implement QI projects.

A Curriculum for Residents to Develop Successful Quality Improvement Projects.

BACKGROUND: Quality improvement (QI) education in residency training has become critical for numerous reasons, but little has been written about factors that lead to successful improvement projects within residency training. METHODS: A quality improvement curriculum for third-year psychiatry residents was developed. The percentage of resident projects that have been successfully implemented was calculated. Residents completed the QI Knowledge Application Tool adapted for psychiatry before and after the curriculum to assess knowledge and skills. RESULTS: Eighteen of 19 resident projects were successfully implemented. QI Knowledge Application Tool scores improved from 4.8 to 8.1 (P = 0.0053) after completion of the curriculum. CONCLUSIONS: Residents are able to implement successful projects and to increase their knowledge and skills in quality improvement when given appropriate resources and incentives.

Response to Disclosure as an Indicator of Competence to Stand Trial.

Ethics guidelines recommend that forensic mental health professionals begin in-person assessments by explaining the nature and purpose of the examination. To learn whether evaluees have understood and can give consent, forensic practitioners may ask evaluees to paraphrase the explanation. This article explores how a forensic evaluee's disclosure response (DR) reveals substantive information relevant to the purposes of a forensic examination. We examined archival data from 255 reports on competence to stand trial (CST) that a Midwest public sector hospital had previously submitted to courts. We classified each evaluee's DR at one of three levels: DR = yes (accurate paraphrasing), DR = no (inability to paraphrase or provide a relevant response), or DR = other (an intermediate level implying a less-than-accurate response). None of the 28 DR = no evaluees was CST, and only 7 (17%) of the 48 DR = other evaluees were CST. Thus, a CST evaluee who cannot paraphrase an examiner's explanation is likely to be incompetent to stand trial, and an examiner would need to adduce a strong argument to support any opinion to the contrary.

A Bayesian approach to mixed group validation of performance validity tests.

Mental health professionals often use structured assessment tools to help detect individuals who are feigning or exaggerating symptoms. Yet estimating the accuracy of these tools is problematic because no "gold standard" establishes whether someone is malingering or not. Several investigators have recommended using mixed group validation (MGV) to estimate the accuracy of malingering measures, but simulation studies show that typical implementations of MGV may yield vague, biased, or logically impossible results. In this article we describe a Bayesian approach to MGV that addresses and avoids these limitations. After explaining the concepts that underlie our approach, we use previously published data on the Test of Memory Malingering (TOMM; Tombaugh, 1996) to illustrate how our method works. Our findings concerning the TOMM's accuracy, which include insights about covariates such as study population and litigation status, are consistent with results that appear in previous publications. Unlike most investigations of the TOMM's accuracy, our findings neither rely on possibly flawed assumptions about subjects' intentions nor assume that experimental simulators can duplicate the behavior of real-world examinees. Our conceptual approach may prove helpful in evaluating the accuracy of many assessment tools used in clinical contexts and psycholegal determinations.

Using Life Stories to Connect Veterans and Providers.

The My Life, My Story patient-centered program uses veterans' personal narratives by veterans to create a strong connection between patients and providers.

High histone acetylation and decreased polycomb repressive complex 2 member levels regulate gene specific transcriptional changes during early embryonic stem cell differentiation induced by retinoic acid.

Histone modifications play a crucial role during embryonic stem (ES) cell differentiation. During differentiation, binding of polycomb repressive complex 2 (PRC2), which mediates trimethylation of lysine 27 on histone H3 (K27me3), is lost on developmental genes that are transcriptionally induced. We observed a global decrease in K27me3 in as little as 3 days after differentiation of mouse ES cells induced by retinoic acid (RA) treatment. The global levels of the histone K27 methyltransferase EZH2 also decreased with RA treatment. A loss of EZH2 binding and K27me3 was observed locally on PRC2 target genes induced after 3 days of RA, including Nestin. In contrast, direct RA-responsive genes that are rapidly induced, such as Hoxa1, showed a loss of EZH2 binding and K27me3 after only a few hours of RA treatment. Following differentiation induced by leukemia inhibitor factor (LIF) withdrawal without RA, Hoxa1 was not transcriptionally activated. Small interfering RNA-mediated knockdown of EZH2 resulted in loss of K27me3 during LIF withdrawal, but the Hoxa1 gene remained transcriptionally silent after loss of this repressive mark. Induction of histone hyperacetylation overrode the repressive K27me3 modification and resulted in Hoxa1 gene expression. Together, these data show that there are multiple temporal phases of derepression of PRC2 target genes during ES cell differentiation and that other epigenetic marks (specifically, increased acetylation of histones H3 and H4), in addition to derepression, are important for gene-specific transcriptional activation. This report demonstrates the temporal interplay of various epigenetic changes in regulating gene expression during early ES cell differentiation.

Dynamic changes in histone H3 phosphoacetylation during early embryonic stem cell differentiation are directly mediated by mitogen- and stress-activated protein kinase 1 via activation of MAPK pathways.

Embryonic stem (ES) cells are pluripotent cells capable of unlimited self-renewal and differentiation into the three embryonic germ layers under appropriate conditions. Mechanisms for control of the early period of differentiation, involving exit from the pluripotent state and lineage commitment, are not well understood. An emerging concept is that epigenetic histone modifications may play a role during this early period. We have found that upon differentiation of mouse ES cells by removal of the cytokine leukemia inhibitory factor, there is a global increase in coupled histone H3 phosphorylation (Ser-10)-acetylation (Lys-14) (H3 phosphoacetylation). We show that this occurs through activation of both the extracellular signal-regulated kinase (ERK) and p38 MAPK signaling pathways. Early ES cell differentiation is delayed using pharmacological inhibitors of the ERK and p38 pathways. One common point of convergence of these pathways is the activation of the mitogen- and stress-activated protein kinase 1 (MSK1). We show here that MSK1 is the critical mediator of differentiation-induced H3 phosphoacetylation using both the chemical inhibitor H89 and RNA interference. Interestingly, inhibition of H3 phosphoacetylation also alters gene expression during early differentiation. These results point to an important role for both epigenetic histone modifications and kinase pathways in modulating early ES differentiation.