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Sudan R.,American College of Education | Sudan R.,Duke University | Lynch T.G.,American College of Education | Lynch T.G.,University of Nebraska Medical Center | And 6 more authors.
Annals of Surgery | Year: 2014

OBJECTIVE:: This report describes the development, initial implementation, and reliability of American College of Surgeons Resident Objective Structured Clinical Examination (ACS OSCE). BACKGROUND:: Variability in clinical knowledge and skills of entering surgery residents has been demonstrated. The ACS OSCE was developed to evaluate and help remediate residents' knowledge and skills in managing patients with life-threatening conditions. METHODS:: A task force of surgeons and professional educators developed 10 standardized clinical case stations, evaluation checklists, and rating scales. Standardized patients (SPs) evaluated each resident's clinical skills (history taking, physical examination, communication, and SP-global scores). Residents completed checklists on diagnosis and management. Coefficient alpha and item-total correlations were used, respectively, to assess internal consistency of metrics and station validity. The resident's overall performance for each station was calculated by combining scores of the individual skills. Analysis of variance compared performance across different institutions. RESULTS:: A total of 103 postgraduate year 1 residents from 7 institutions completed the OSCE. Reliability coefficients of skills ranged from 0.38 for diagnosis to 0.68 for global scores. For overall performance on individual stations, the reliability coefficients ranged from 0.51 to 0.82. Using total percent correct scores from highly reliable stations (α > 0.8), wide variability in resident performance was demonstrated within and between the 7 institutions. CONCLUSIONS:: The ACS OSCE was successfully implemented across diverse institutions. It had moderate reliability and demonstrated variability among entering surgery residents. The ACS OSCE is now available for broader implementation. It should help reduce resident variability and address the requirements of Accreditation Council for Graduate Medical Education for resident supervision.Copyright © 2014 by Lippincott Williams & Wilkins.


Dodmane P.R.,University of Nebraska Medical Center | Schulte N.A.,University of Nebraska Medical Center | Heires A.J.,University of Nebraska Medical Center | Band H.,Eppley Institute for Research in Cancer and Allied Diseases | And 3 more authors.
American Journal of Respiratory Cell and Molecular Biology | Year: 2011

A subset of workers in swine confinement facilities develops chronic respiratory disease. An aqueous extract of dust from these facilities (hogbarn dust extract [HDE]) induces IL-6 and IL-8 release and several other responses in isolated airway epithelial cells. The cell membrane receptors by which HDE initiates these responses have not been identified. Because several other inhaled agents induce airway epithelial cell responses through epidermal growth factor receptor (EGFR) activation, we hypothesized that HDE would activate EGFRs and that EGFRs would be required for some of the responses to HDE. Exposure of Beas-2B cells to HDE caused EGFR phosphorylation and downstream ERK activation, and both responses were blocked by the EGFR-selective kinase inhibitor AG1478. AG1478 and EGFR-neutralizing antibody reduced HDE-stimulated IL-6 and IL-8 release by about half. Similar EGFR phosphorylation and requirement of EGFRs formaximal IL-6 and IL-8 release were found with primary isolates of human bronchial epithelial cells. Because HDE-stimulated IL-6 and IL-8 release involve the Ca 2+-dependent protein kinase Cα, we hypothesized that HDE would induce intracellular Ca 2+ mobilization. HDE exposure induced intracellular Ca 2+ mobilization in Beas-2B cells and in primary cell isolates, but this response was neither mimicked by EGF nor inhibited by AG1478. Thus, HDE activates EGFRs and their downstream signaling, and EGFR activation is required for some but not all airway epithelial cell responses to HDE.


Petrosyan A.,Veterans Administration Nebraska Western Iowa Health Care System | Petrosyan A.,University of Nebraska Medical Center | Cheng P.-W.,Veterans Administration Nebraska Western Iowa Health Care System | Cheng P.-W.,University of Nebraska Medical Center
Cell Stress and Chaperones | Year: 2014

The Golgi apparatus is a highly dynamic organelle which frequently undergoes morphological changes in certain normal physiological processes or in response to stress. The mechanisms are largely not known. We have found that heat shock of Panc1 cells expressing core 2 N-acetylglucosaminyltransferase-M (Panc1-C2GnT-M) induces Golgi disorganization by increasing non-muscle myosin IIA (NMIIA)-C2GnT-M complexes and polyubiquitination and proteasomal degradation of C2GnT-M. These effects are prevented by inhibition or knockdown of NMIIA. Also, the speed of Golgi fragmentation induced by heat shock is found to be positively correlated with the levels of C2GnT-M in the Golgi. The results are reproduced in LNCaP cells expressing high levels of two endogenous glycosyltransferases-core 2 N-acetylglucosaminyltransferase-L:1 and β-galactoside:α2-3 sialyltransferase 1. Further, during recovery after heat shock, Golgi reassembly as monitored by a Golgi matrix protein giantin precedes the return of C2GnT-M to the Golgi. The results are consistent with the roles of giantin as a building block of the Golgi architecture and a docking site for transport vesicles carrying glycosyltransferases. In addition, inhibition/depletion of HSP70 or HSP90 in Panc1-C2GnT-M cells also causes an increase of NMIIA-C2GnT-M complexes and NMIIA-mediated Golgi fragmentation but results in accumulation or degradation of C2GnT-M, respectively. These results can be explained by the known functions of these two HSP: participation of HSP90 in protein folding and HSP70 in protein folding and degradation. We conclude that NMIIA is the master regulator of Golgi fragmentation induced by heat shock or inhibition/depletion of HSP70/90. © 2013 Cell Stress Society International.


Almquist D.,Veterans Administration Nebraska Western Iowa Health Care System | Mosalpuria K.,Veterans Administration Nebraska Western Iowa Health Care System | Ganti A.K.,University of Nebraska Medical Center
Journal of Oncology Practice | Year: 2016

Limited-stage small-cell lung cancer (SCLC) occurs in only one third of patients with SCLC, but it is potentially curable. Combined-modality therapy (chemotherapy and radiotherapy) has long been themainstay of therapy for this condition, butmore recent data suggest a role for surgery in early-stage disease. Prophylactic cranial irradiation seems to improve outcomes in patients who have responded to initial therapy. This review addresses the practical aspects of staging and treatment of patients with limited-stage SCLC. © 2016 by American Society of Clinical Oncology.


Chachadi V.B.,Veterans Administration Nebraska Western Iowa Health Care System | Chachadi V.B.,University of Nebraska Medical Center | Ali M.F.,Veterans Administration Nebraska Western Iowa Health Care System | Ali M.F.,University of Nebraska Medical Center | And 2 more authors.
PLoS ONE | Year: 2013

Sialyl Lewis antigens are selectin ligands involved in leukocyte trafficking and cancer metastasis. Biosynthesis of these selectin ligands occurs by the sequential actions of several glycosyltransferases in the Golgi apparatus following synthesis of the protein backbone in the endoplasmic reticulum. In this study, we examine how the synthesis of sialyl Lewis a (sLea) is regulated in prostatic cells and identify a mucin that carries this glycotope. We treat human prostatic cells including one normal and three cancerous cells with histone deacetylase inhibitors, valproic acid, tricostatin A (TSA), and suberoylanilide hydroxamic acid (SAHA), and then monitor the expression of sLea. We have found that SAHA enhances the production of sLea in normal prostatic RWPE-1 cells but not prostatic cancer cells. Employing siRNA technology and co-immunoprecipitation, we show that the sLea is associated with MUC1, which is confirmed by confocal immunofluorescence microscopy and proximity ligation assay. The SAHA-induced production of sLea in RWPE-1 cells is resulted from upregulation of B3GALT1 gene via enhancement of acetylated histone-3 and histone-4. Interestingly, PC3 and LNCaP C-81 cells do not produce detectable amounts of sLea despite expressing high levels of B3GALT1. However, the MUC1-associated sLea is generated in these cells after introduction of MUC1 cDNA. We conclude that the synthesis of sLea is controlled by not only peptide backbone of the glycoprotein but also glycoprotein-specific glycosyltransferases involved in the synthesis of sLea. Further, the SAHA induction of this selectin ligand in normal prostatic cells may pose a potentially serious side effect of this drug recently approved by the US Food and Drug Administration.


PubMed | Veterans Administration Nebraska Western Iowa Health Care System
Type: Journal Article | Journal: PloS one | Year: 2013

Sialyl Lewis antigens are selectin ligands involved in leukocyte trafficking and cancer metastasis. Biosynthesis of these selectin ligands occurs by the sequential actions of several glycosyltransferases in the Golgi apparatus following synthesis of the protein backbone in the endoplasmic reticulum. In this study, we examine how the synthesis of sialyl Lewis a (sLe(a)) is regulated in prostatic cells and identify a mucin that carries this glycotope. We treat human prostatic cells including one normal and three cancerous cells with histone deacetylase inhibitors, valproic acid, tricostatin A (TSA), and suberoylanilide hydroxamic acid (SAHA), and then monitor the expression of sLe(a). We have found that SAHA enhances the production of sLe(a) in normal prostatic RWPE-1 cells but not prostatic cancer cells. Employing siRNA technology and co-immunoprecipitation, we show that the sLe(a) is associated with MUC1, which is confirmed by confocal immunofluorescence microscopy and proximity ligation assay. The SAHA-induced production of sLe(a) in RWPE-1 cells is resulted from upregulation of B3GALT1 gene via enhancement of acetylated histone-3 and histone-4. Interestingly, PC3 and LNCaP C-81 cells do not produce detectable amounts of sLe(a) despite expressing high levels of B3GALT1. However, the MUC1-associated sLe(a) is generated in these cells after introduction of MUC1 cDNA. We conclude that the synthesis of sLe(a) is controlled by not only peptide backbone of the glycoprotein but also glycoprotein-specific glycosyltransferases involved in the synthesis of sLe(a). Further, the SAHA induction of this selectin ligand in normal prostatic cells may pose a potentially serious side effect of this drug recently approved by the US Food and Drug Administration.

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