Improving attending rounds: Qualitative reflections from multidisciplinary providers.

BACKGROUND: Attending rounds, the time for the attending physician and the team to discuss the team's patients, take place at teaching hospitals every day, often with little standardization. OBJECTIVE: This hypothesis-generating qualitative study sought to solicit improvement recommendations for standardizing attending rounds from the perspective of a multi-disciplinary group of providers. METHODS: Attending physicians, housestaff (residents and interns), medical students, nurses and pharmacists at an academic medical center participated in a quality improvement initiative between January and April 2013. Participants completed an individual or focus group interview or an e-mail survey with three open-ended questions: (1) What are poor or ineffective practices for attending rounds? (2) How would you change attending rounds structure and function? (3) What do you consider best practices for attending rounds? We undertook content analysis to summarize each clinical stakeholder group's improvement recommendations. RESULTS: Sixty stakeholders participated in our study including 23 attending hospitalists, 24 housestaff, 7 medical students, 2 pharmacists and 4 nurses. Key improvement recommendations included (1) performing a pre-rounds huddle, (2) planning of the visit schedule based on illness or pending discharge, (3) real-time order writing, (4) patient involvement in rounds with shared decision-making, (5) bedside nurse inclusion and (6) minimizing interruption of intern or student presentations. CONCLUSIONS: The practice improvement recommendations identified in this study will require deliberate systems changes and training to implement, and they warrant rigorous evaluation to determine their impact on the clinical and educational goals of rounds.

No significant association of 14 candidate genes with schizophrenia in a large European ancestry sample: implications for psychiatric genetics.

OBJECTIVE: The authors carried out a genetic association study of 14 schizophrenia candidate genes (RGS4, DISC1, DTNBP1, STX7, TAAR6, PPP3CC, NRG1, DRD2, HTR2A, DAOA, AKT1, CHRNA7, COMT, and ARVCF). This study tested the hypothesis of association of schizophrenia with common single nucleotide polymorphisms (SNPs) in these genes using the largest sample to date that has been collected with uniform clinical methods and the most comprehensive set of SNPs in each gene. METHOD: The sample included 1,870 cases (schizophrenia and schizoaffective disorder) and 2,002 screened comparison subjects (i.e. controls), all of European ancestry, with ancestral outliers excluded based on analysis of ancestry-informative markers. The authors genotyped 789 SNPs, including tags for most common SNPs in each gene, SNPs previously reported as associated, and SNPs located in functional domains of genes such as promoters, coding exons (including nonsynonymous SNPs), 3' untranslated regions, and conserved noncoding sequences. After extensive data cleaning, 648 SNPs were analyzed for association of single SNPs and of haplotypes. RESULTS: Neither experiment-wide nor gene-wide statistical significance was observed in the primary single-SNP analyses or in secondary analyses of haplotypes or of imputed genotypes for additional common HapMap SNPs. Results in SNPs previously reported as associated with schizophrenia were consistent with chance expectation, and four functional polymorphisms in COMT, DRD2, and HTR2A did not produce nominally significant evidence to support previous evidence for association. CONCLUSIONS: It is unlikely that common SNPs in these genes account for a substantial proportion of the genetic risk for schizophrenia, although small effects cannot be ruled out.

DTNBP1 (Dystrobrevin binding protein 1) and schizophrenia: association evidence in the 3' end of the gene.

OBJECTIVES: Dysbindin (DTNBP1) has been identified as a susceptibility gene for schizophrenia (SZ) through a positional approach. However, a variety of single nucleotide polymorphisms (SNPs) and haplotypes, in different parts of the gene, have been reported to be associated in different samples, and a precise molecular mechanism of disease remains to be defined. We have performed an association study with two well-characterized family samples not previously investigated at the DTNBP1 locus. METHODS: We examined 646 subjects in 136 families with SZ, largely of European ancestry (EA), genotyping 26 SNPs in DTNBP1. RESULTS: Three correlated markers (rs875462, rs760666, and rs7758659) at the 3' region of DTNBP1 showed evidence for association to SZ (p = 0.004), observed in both the EA (p = 0.031) and the African American (AA) subset (p = 0.045) with the same over-transmitted allele. The most significant haplotype in our study was rs7758659-rs3213207 (global p = 0.0015), with rs3213207 being the most frequently reported associated marker in previous studies. A non-conservative missense variant (Pro272Ser) in the 3' region of DTNBP1 that may impair DTNBP1 function was more common in SZ probands (8.2%) than in founders (5%) and in dbSNP (2.1%), but did not reach statistical significance. CONCLUSION: Our results provide evidence for an association of SZ with SNPs at the 3' end of DTNBP1 in the samples studied.