Records |
Author |
Cole, D.C.; Giordano, C.R.; Vasilopoulos, T.; Fahy, B.G. |
Title |
Resident Physicians Improve Nontechnical Skills When on Operating Room Management and Leadership Rotation |
Type |
Journal Article |
Year |
2017 |
Publication |
Anesthesia and Analgesia |
Abbreviated Journal |
Anesth Analg |
Volume |
124 |
Issue |
1 |
Pages |
300-307 |
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Abstract |
BACKGROUND: Anesthesiology residency primarily emphasizes the development of medical knowledge and technical skills. Yet, nontechnical skills (NTS) are also vital to successful clinical practice. Elements of NTS are communication, teamwork, situational awareness, and decision making. METHODS: The first 10 consecutive senior residents who chose to participate in this 2-week elective rotation of operating room (OR) management and leadership training were enrolled in this study, which spanned from March 2013 to March 2015. Each resident served as the anesthesiology officer of the day (AOD) and was tasked with coordinating OR assignments, managing care for 2 to 4 ORs, and being on call for the trauma OR; all residents were supervised by an attending AOD. Leadership and NTS techniques were taught via a standardized curriculum consisting of leadership and team training articles, crisis management text, and daily debriefings. Resident self-ratings and attending AOD and charge nurse raters used the Anaesthetists' Non-Technical Skills (ANTS) scoring system, which involved task management, situational awareness, teamwork, and decision making. For each of the 10 residents in their third year of clinical anesthesiology training (CA-3) who participated in this elective rotation, there were 14 items that required feedback from resident self-assessment and OR raters, including the daily attending AOD and charge nurse. Results for each of the items on the questionnaire were compared between the beginning and the end of the rotation with the Wilcoxon signed-rank test for matched samples. Comparisons were run separately for attending AOD and charge nurse assessments and resident self-assessments. Scaled rankings were analyzed for the Kendall coefficient of concordance (omega) for rater agreement with associated chi and P value. RESULTS: Common themes identified by the residents during debriefings were recurrence of challenging situations and the skills residents needed to instruct and manage clinical teams. For attending AOD and charge nurse assessments, resident performance of NTS improved from the beginning to the end of the rotation on 12 of the 14 NTS items (P < .05), whereas resident self-assessment improved on 3 NTS items (P < .05). Interrater reliability (across the charge nurse, resident, and AOD raters) ranged from omega = .36 to .61 at the beginning of the rotation and omega = .27 to .70 at the end of the rotation. CONCLUSIONS: This rotation allowed for teaching and resident assessment to occur in a way that facilitated resident education in several of the skills required to meet specific milestones. Resident physicians are able to foster NTS and build a framework for clinical leadership when completing a 2-week senior elective as an OR manager. |
Address |
From the Department of Anesthesiology, University of Florida, College of Medicine, Gainesville, Fla |
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0003-2999 |
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PMID:27918336 |
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ref @ user @ |
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95061 |
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Author |
Polex-Wolf, J.; Yeo, G.S.H.; O'Rahilly, S. |
Title |
Impaired prohormone processing: a grand unified theory for features of Prader-Willi syndrome? |
Type |
Journal Article |
Year |
2017 |
Publication |
The Journal of Clinical Investigation |
Abbreviated Journal |
J Clin Invest |
Volume |
127 |
Issue |
1 |
Pages |
98-99 |
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Abstract |
Prader-Willi syndrome (PWS) is a complex disorder that manifests with an array of phenotypes, such as hypotonia and difficulties in feeding during infancy and reduced energy expenditure, hyperphagia, and developmental delays later in life. While the genetic cause has long been known, it is still not clear how mutations at this locus produce this array of phenotypes. In this issue of the JCI, Burnett and colleagues used a comprehensive approach to gain insight into how PWS-associated mutations drive disease. Using neurons derived from PWS patient induced pluripotent stem cells (iPSCs) and mouse models, the authors provide evidence that neuroendocrine PWS-associated phenotypes may be linked to reduced expression of prohormone convertase 1 (PC1). While these compelling results support a critical role for PC1 deficiency in PWS, more work needs to be done to fully understand how and to what extent loss of this prohormone processing enzyme underlies disease manifestations in PWS patients. |
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0021-9738 |
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PMID:27941250 |
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ref @ user @ |
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95907 |
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Author |
Tahara, T.; Hirata, I.; Nakano, N.; Nagasaka, M.; Nakagawa, Y.; Shibata, T.; Ohmiya, N. |
Title |
Comprehensive DNA Methylation Profiling of Inflammatory Mucosa in Ulcerative Colitis |
Type |
Journal Article |
Year |
2017 |
Publication |
Inflammatory Bowel Diseases |
Abbreviated Journal |
Inflamm Bowel Dis |
Volume |
23 |
Issue |
1 |
Pages |
165-173 |
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Abstract |
INTRODUCTION: Aberrant DNA methylation frequently occurs in the inflammatory mucosa in ulcerative colitis (UC) and is involved in UC-related tumorigenesis. We performed comprehensive DNA methylation profiling of the promoter regions of the inflamed rectal mucosae of patients with UC. DESIGN: The methylation status of the promoter CpG islands (CGIs) of 45 cancer/inflammation or age-related candidate genes and the LINE1 repetitive element were examined in the colonic mucosae of 84 cancer-free patients with UC by bisulfite pyrosequencing. Methylation status of selected genes (DPYS, N33, MIR1247, GSTP1, and SOX11) was also determined in 14 neoplastic lesions (5 with high-grade dysplasia and 9 with carcinoma) and 8 adjacent tissues derived from 12 patients. An Infinium HumanMethylation450 BeadChip array was used to characterize the methylation status of >450,000 CpG sites for 10 patients with UC. RESULTS: Clustering analysis based on the methylation status of the candidate genes clearly distinguished the inflammatory samples from the noninflammatory samples. The hypermethylation of the promoter CGIs strongly correlated with increased disease duration, which is a known risk factor for the development of colon cancer. Genome-wide methylation analyses revealed a high rate of hypermethylation in the severe phenotype of UC, particularly at the CGIs. Exclusively hypermethylated promoter CGIs in the severe phenotypes were significantly related to genes involved in biosynthetic processes, the regulation of metabolic processes, and nitrogen compound metabolic processes. CONCLUSION: Our findings suggest the potential utility of DNA methylation as a molecular marker and therapeutic target for UC-related tumorigenesis. |
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*Department of Gastroenterology, Fujita Health University School of Medicine, Toyoake, Japan; and daggerDepartment of Gastroenterology, Tanimukai Hospital Japan, Nishinomiya, Japan |
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1078-0998 |
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PMID:27930411 |
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ref @ user @ |
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96375 |
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Guerrero, P.A.; Tchaicha, J.H.; Chen, Z.; Morales, J.E.; McCarty, N.; Wang, Q.; Sulman, E.P.; Fuller, G.; Lang, F.F.; Rao, G.; McCarty, J.H. |
Title |
Glioblastoma stem cells exploit the alphavbeta8 integrin-TGFbeta1 signaling axis to drive tumor initiation and progression |
Type |
Journal Article |
Year |
2017 |
Publication |
Oncogene |
Abbreviated Journal |
Oncogene |
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Glioblastoma (GBM) is a primary brain cancer that contains populations of stem-like cancer cells (GSCs) that home to specialized perivascular niches. GSC interactions with their niche influence self-renewal, differentiation and drug resistance, although the pathways underlying these events remain largely unknown. Here, we report that the integrin alphavbeta8 and its latent transforming growth factor beta1 (TGFbeta1) protein ligand have central roles in promoting niche co-option and GBM initiation. alphavbeta8 integrin is highly expressed in GSCs and is essential for self-renewal and lineage commitment in vitro. Fractionation of beta8high cells from freshly resected human GBM samples also reveals a requirement for this integrin in tumorigenesis in vivo. Whole-transcriptome sequencing reveals that alphavbeta8 integrin regulates tumor development, in part, by driving TGFbeta1-induced DNA replication and mitotic checkpoint progression. Collectively, these data identify the alphavbeta8 integrin-TGFbeta1 signaling axis as crucial for exploitation of the perivascular niche and identify potential therapeutic targets for inhibiting tumor growth and progression in patients with GBM.Oncogene advance online publication, 7 August 2017; doi:10.1038/onc.2017.248. |
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Department of Neurosurgery, M. D. Anderson Cancer Center, Houston, TX, USA |
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0950-9232 |
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PMID:28783169 |
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no |
Call Number |
ref @ user @ |
Serial |
96572 |
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Author |
Magrath, J.W.; Kim, Y. |
Title |
Salinomycin's potential to eliminate glioblastoma stem cells and treat glioblastoma multiforme (Review) |
Type |
Journal Article |
Year |
2017 |
Publication |
International Journal of Oncology |
Abbreviated Journal |
Int J Oncol |
Volume |
51 |
Issue |
3 |
Pages |
753-759 |
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Abstract |
Glioblastoma multiforme (GBM) is the most common and deadliest form of primary brain tumor. Despite treatment with surgery, radiotherapy, and chemotherapy with the drug temozolomide, the expected survival after diagnosis remains low. The median survival is only 14.6 months and the two-year survival is a mere 30%. One reason for this is the heterogeneity of GBM including the presence of glioblastoma cancer stem cells (GSCs). GSCs are a subset of cells with the unique ability to proliferate, differentiate, and create tumors. GSCs are resistant to chemotherapy and radiation and thought to play an important role in recurrence. In order to effectively treat GBM, a drug must be identified that can kill GSCs. The ionophore salinomycin has been shown to kill cancer stem cells and is therefore a promising future treatment for GBM. This study focuses on salinomycin's potential to treat GBM including its ability to reduce the CSC population, its toxicity to normal brain cells, its mechanism of action, and its potential for combination treatment. |
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Department of Chemical and Biological Engineering, The University of Alabama, Tuscaloosa, AL 35487-0203, USA |
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1019-6439 |
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PMID:28766685 |
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ref @ user @ |
Serial |
96573 |
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