Association of Intern and Resident Burnout With Self-Reported Medical Errors.

Association of Intern and Resident Burnout with Self-Reported Medical Errors.

Filed under: Depression Treatment

Korean J Fam Med. 2013 Jan; 34(1): 36-42
Kang EK, Lihm HS, Kong EH

BACKGROUND: Burnout is a common problem for interns and residents. It may be related to medical error, but little is known about this relationship. The purpose of this study was to determine the association between burnout and perceived medical errors among interns and residents. METHODS: The study group consisted of interns and residents working in a university hospital in Busan. Data were provided by 86 (58.5%) of 147 interns and residents. They completed a questionnaire including self-assessment of medical errors, a linear analog self-assessment of overall quality of life (QOL), fatigue, the Epworth Sleepiness Scale (ESS) score, the Maslach Burnout Inventory, and a validated depression screening tool. RESULTS: According to univariate logistic regression analyses, there was an association between perceived medical errors and fatigue (odds ratio [OR], 1.37 per unit increase; 95% confidence interval [CI], 1.12 to 1.69; P < 0.003) and ESS scores (OR, 1.13 per unit increase; 95% CI, 1.03 to 1.23; P < 0.009). Perceived medical errors were also associated with burnout (ORs per 1-unit change; emotional exhaustion OR, 1.07; 95% CI, 1.02 to 1.13; P < 0.005; depersonalization OR, 1.11; 95% CI, 1.02 to 1.21; P < 0.013), a negative depression screen (OR, 0.29; 95% CI, 0.11 to 0.76; P < 0.013), and overall QOL (OR, 0.80; 95% CI, 0.70 to 0.98; P < 0.033). In multivariate logistic regression analyses, an association was identified between perceived medical errors and emotional exhaustion (OR, 1.06; 95% CI, 1.00 to 1.11; P < 0.046) when adjusted for ESS, and depersonalization (OR, 1.01; 95% CI, 1.01 to 1.19; P < 0.04) when adjusted for fatigue. CONCLUSION: Higher levels of burnout among interns and residents were associated with perceived medical errors. HubMed – depression

 

The effects of an insulin-glucose-potassium (IGK) pretreatment on the bupivacaine cardiotoxicity.

Filed under: Depression Treatment

Korean J Anesthesiol. 2013 Jan; 64(1): 47-53
Kim JT, Yang SM, Lee KH

BACKGROUND: The purpose of this study is to evaluate the effect of an IGK pretreatment on the cardiotoxicity of bupivacaine. METHODS: Twenty-one anesthetized mongrel dogs were randomly divided into the following three groups: the control group (CG, n = 7), the treatment group (TG, n = 7) and the pretreatment group (PTG, n = 7). For the 30 min of pretreatment period, CG and TG received normal saline, while PTG received an IV bolus of insulin 2 U/kg, followed by an IGK infusion (2 U/kg/hr of insulin, 0.5-1.5 g/kg/hr of glucose, 1-2 mEq/kg/hr of KCl). The bupivacaine infusion was started at the rate of 0.5 mg/kg/min in all groups after the pretreatment period. CG received normal saline only. In TG, insulin (2 U/kg) was injected simultaneously with bupivacaine infusion, followed by the IGK infusion as with PTG. The hemodynamic variables and the time duration to reach the mean arterial pressure (MAP) of 60 mmHg were compared. RESULTS: The bupivacaine infusion decreased the cardiac index, MAP, and heart rate in all three groups. Although insulin concentration was higher in TG than in PTG during bupivacaine infusion, the hemodynamic variables in PTG decreased at the slowest rate. The time taken to reach MAP of 60 mmHg in PTG, TG, and CG was 51.4 ± 8.5, 36.4 ± 9.6, and 27.1 ± 8.7 min, respectively (P < 0.05). CONCLUSIONS: IGK delays the bupivacaine-induced cardiac depression. However, a pretreatment with IGK is more effective in delaying the bupivacaine-induced hypotension than simultaneous administration, regardless of insulin concentration. HubMed – depression

 

Structural and Functional Analysis of the DEAF-1 and BS69 MYND Domains.

Filed under: Depression Treatment

PLoS One. 2013; 8(1): e54715
Kateb F, Perrin H, Tripsianes K, Zou P, Spadaccini R, Bottomley M, Franzmann TM, Buchner J, Ansieau S, Sattler M

DEAF-1 is an important transcriptional regulator that is required for embryonic development and is linked to clinical depression and suicidal behavior in humans. It comprises various structural domains, including a SAND domain that mediates DNA binding and a MYND domain, a cysteine-rich module organized in a Cys(4)-Cys(2)-His-Cys (C4-C2HC) tandem zinc binding motif. DEAF-1 transcription regulation activity is mediated through interactions with cofactors such as NCoR and SMRT. Despite the important biological role of the DEAF-1 protein, little is known regarding the structure and binding properties of its MYND domain.Here, we report the solution structure, dynamics and ligand binding of the human DEAF-1 MYND domain encompassing residues 501-544 determined by NMR spectroscopy. The structure adopts a ??? fold that exhibits tandem zinc-binding sites with a cross-brace topology, similar to the MYND domains in AML1/ETO and other proteins. We show that the DEAF-1 MYND domain binds to peptides derived from SMRT and NCoR corepressors. The binding surface mapped by NMR titrations is similar to the one previously reported for AML1/ETO. The ligand binding and molecular functions of the related BS69 MYND domain were studied based on a homology model and mutational analysis. Interestingly, the interaction between BS69 and its binding partners (viral and cellular proteins) seems to require distinct charged residues flanking the predicted MYND domain fold, suggesting a different binding mode. Our findings demonstrate that the MYND domain is a conserved zinc binding fold that plays important roles in transcriptional regulation by mediating distinct molecular interactions with viral and cellular proteins.
HubMed – depression

 

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