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1.
Eval Health Prof ; 31(4): 419-36, 2008 Dec.
Article in English | MEDLINE | ID: mdl-18842619

ABSTRACT

Assessments of temporal bone dissection performance among otolaryngology residents have not been adequately developed. At the Ohio State College of Medicine, an instrument (Welling Scale, Version 1 [WS1]) is used to evaluate residents' end-product performance after drilling a temporal bone. In this study, the authors evaluate the components that contribute to measurement error using this scale. Generalizability theory was used to reveal components of measurement error that allow for better understanding of test results. A major component of measurement error came from inconsistency in performance across the two cadaveric test bones each resident was assigned. In contrast, ratings of performance using the WS1 were highly consistent across raters and rating sessions within raters. The largest source of measurement error was caused by residents' inconsistent performance across bones. Rater disagreement introduced only small error into scores. The WS1 provides small measurement error, with two raters and two bones for each participant.


Subject(s)
Educational Measurement/methods , Otolaryngology/education , Otorhinolaryngologic Surgical Procedures/education , Clinical Competence , Humans , Internship and Residency , Otorhinolaryngologic Surgical Procedures/standards , Reproducibility of Results
2.
Laryngoscope ; 117(10): 1803-8, 2007 Oct.
Article in English | MEDLINE | ID: mdl-17721407

ABSTRACT

OBJECTIVE: To determine the inter- and intrarater reliability of using a new scale (Welling scale) for resident evaluation of temporal bone dissection performance. STUDY DESIGN: Prospective, double-blinded, randomized trial. METHODS: Twelve residents in otolaryngology (postgraduate year [PGY] 2-5) drilled 26 temporal bones (21 cadaveric, 5 plastic) with the objective to perform a complete mastoidectomy with facial recess approach. These bones were then rated using the Welling scale by six independent raters on two separate occasions (4-6 wk apart). Raters were blinded to PGY year. The Kappa statistic was calculated for inter- and intrarater reliability. RESULTS: Intrarater agreement was high for all raters, ranging from kappa = 0.65 to 0.72 (all P < .001), whereas the interrater agreement scores were more moderate (range, kappa = 0.49-0.64; all P < .01). CONCLUSION: The Welling scale can be used reliably to assess temporal bone dissection performance where performance is measured by assessment of end product (mastoidectomy with facial recess approach).


Subject(s)
Clinical Competence , Mastoid/surgery , Otolaryngology/education , Otorhinolaryngologic Surgical Procedures/methods , Surveys and Questionnaires , Temporal Bone/surgery , Cadaver , Double-Blind Method , Educational Measurement , Humans , Internship and Residency , Prospective Studies
3.
Surg Obes Relat Dis ; 2(2): 105-11, 2006.
Article in English | MEDLINE | ID: mdl-16925332

ABSTRACT

BACKGROUND: Increased morbidity is associated with increasing severity of obesity. However, among morbidly obese patients, comorbid prevalence has been reported primarily in the bariatric surgical literature. This study compares demographic characteristics and selected comorbid conditions of morbidly obese patients discharged after surgical obesity procedures and morbidly obese patients discharged after all other hospital procedures. METHODS: The 2002 National Hospital Discharge Survey (a nationally representative sample of hospital discharge records) and the International Classification of Diseases, 9th Revision, Clinical Modification were used to identify and describe all morbidly obese patient discharges (n = 3,473) and to quantify the prevalence of selected obesity-related comorbid conditions. RESULTS: Compared with all other morbidly obese patients, the obesity surgery patients (n = 833) were younger (median, 42 vs 48 years; range, 17 to 67) and more female (82.3% vs. 63.7%), with higher rates of sleep apnea (24.0% vs. 11.8%), osteoarthritis (22.9% vs. 11.8%), and gastroesophageal reflux disease (27.7% vs. 11.7%) (all P < .001). The prevalence of type 2 diabetes mellitus was lower in the obesity surgery patients (16.1% vs. 24.3%; P = .003), whereas the rates of hypertension (45.9% vs. 41.0%; P = .13) and asthma (9.6% vs. 12.0%; P = .26) were similar in the two groups. CONCLUSIONS: Demographic characteristics and comorbid prevalence of morbidly obese patients discharged after obesity surgery are consistent with reports in the bariatric surgical literature. Obesity surgery patients had a higher prevalence of some comorbid conditions. Possible explanations for this include preferential diagnosis, differential diagnostic coding, or increased severity of morbid obesity. Advancing surgical and insurance guidelines for bariatric surgery will require clinical data that accurately describe and quantify the demographic distribution of obesity and the associated burden of disease.


Subject(s)
Comorbidity , Obesity, Morbid , Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Obesity, Morbid/epidemiology , Obesity, Morbid/surgery , Patient Discharge , Prevalence , United States/epidemiology
4.
Int J Oncol ; 24(6): 1473-80, 2004 Jun.
Article in English | MEDLINE | ID: mdl-15138590

ABSTRACT

The mitogen-activated protein kinase (MAPK) cascade is a critical component in the regulation of cell survival and proliferation decisions. In breast carcinoma cells, activation of the p38-MAPK member of this family occurs in response to pro-inflammatory cytokines and cellular stress. The involvement of p38-MAPK in the activation of the transcription factor, NF-kappaB, suggests a potential role and mechanism for regulation of cell survival and drug resistance. Generation of the resistant MCF-7 variant (MCF-7TN-R) was achieved by prolonged exposure of MCF-7N cells to increasing concentrations of TNF. Differences in MAPK activation and function in the MCF-7 cell variants were determined. The role of the p38-MAPK pathway in regulation of resistance was determined using pharmacological (SB 203580) or molecular [Dominant Inhibitory (DI)-p38] inhibition. The effect of p38 inhibition on NF-kappaB transcriptional activation was analyzed. As compared to the sensitive MCF-7N parent cell line, the MCF-7TN-R cell line displayed significant resistance to TNF- and TRAIL-induced cell death. Analysis of the expression and phosphorylation of members of the MAPK family revealed an increased basal activation of p38 in the MCF-7TN-R variant. The p38-mediated phosphorylation and transcriptional activity were suppressed by pharmacologic inhibition with SB 230580. Treatment of MCF-7TN-R cells with SB partially restored sensitivity to TNF-induced cell death. In addition, use of a DI-p38 construct with or without the addition to TNF induced cell death, thus restoring TNF-sensitivity to these cells. The ability of p38 inhibition to restore apoptotic sensitivity was correlated with suppression of the TNF-induced cell survival pathway, NF-kappaB. The increased activation of p38-MAPK in MCF-7TN-R cells demonstrates that this signaling pathway through activation of NF-kappaB is an important route for control of resistance to cell death in breast carcinoma. Molecular and pharmacological inhibition of p38-MAPK signaling may represent a mechanism for sensitizing cancer cells to chemotherapeutic regimens and restoration of apoptotic signaling.


Subject(s)
Apoptosis/drug effects , Breast Neoplasms/metabolism , Drug Resistance, Neoplasm , Membrane Glycoproteins/pharmacology , Signal Transduction/drug effects , Tumor Necrosis Factor-alpha/pharmacology , p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors , Apoptosis Regulatory Proteins , Breast Neoplasms/pathology , Enzyme Activation/drug effects , Enzyme Inhibitors/pharmacology , Female , Genes, Dominant , Humans , Luciferases/metabolism , NF-kappa B/metabolism , Phosphorylation/drug effects , TNF-Related Apoptosis-Inducing Ligand , Transcription, Genetic , Tumor Cells, Cultured
5.
Surgery ; 132(2): 293-301, 2002 Aug.
Article in English | MEDLINE | ID: mdl-12219026

ABSTRACT

BACKGROUND: Components of the mitogen-activated protein kinase (MAPK) cascade have been implicated in apoptotic regulation. This study used gene expression profiling analysis to identify and implicate mitogen-activated protein kinase kinase (MEK5)-BMK1 (big mitogen-activated kinase-1)/extracellular signal related protein kinase (ERK5) pathway as a novel target involved in chemoresistance. METHODS: Differential gene expression between apoptotically sensitive (APO+) and apoptotically resistant (APO-) MCF-7 cell variants was determined by using microarray and confirmed by reverse transcriptase- polymerase chain reaction (RT-PCR). An apoptotic/viability reporter gene assay was used to deter-mine the effects of the transfection of a dominant-negative mutant of BMK1 (BMK1/DN) in conjunction with apoptotic-inducing agents (etoposide, tumor necrosis factor-alpha [TNF], or TNF-related apoptosis-inducing ligand [TRAIL]), with or without phorbol ester (PMA). RESULTS: Of the 1186 genes detected through microarray analysis, MEK5 was increased 22-fold in APO- cells. Overexpression of MEK5 was confirmed by using RT-PCR analysis. Expression of BMK1/DN alone resulted in a dose-dependent increase in cell death versus control (P <.05). In addition, BMK1/DN enhanced the sensitivity of MCF-7 cells to treatment-induced cell death (P <.05). The ability of PMA to partially suppress TRAIL- and TNF-induced cell death was inhibited by BMK1/DN. However, only TRAIL-induced activity suppression reached statistical significance (P <.05). CONCLUSIONS: The overexpression of MEK5 in APO- MCF-7 breast carcinoma cells shows that this MAPK signaling protein represents a potent survival molecule. Molecular inhibition of MEK5 signaling may represent a mechanism for sensitizing cancer cells to chemotherapeutic regimens.


Subject(s)
Breast Neoplasms , Drug Resistance, Neoplasm/genetics , Mitogen-Activated Protein Kinase Kinases/genetics , Antineoplastic Agents/pharmacology , Antineoplastic Agents, Phytogenic/pharmacology , Apoptosis/drug effects , Apoptosis/genetics , Apoptosis Regulatory Proteins , Carcinogens/pharmacology , Cell Survival/drug effects , Cell Survival/genetics , Etoposide/pharmacology , Female , Humans , MAP Kinase Kinase 5 , Membrane Glycoproteins/pharmacology , Mitogen-Activated Protein Kinase 7 , Mitogen-Activated Protein Kinases/genetics , Oligonucleotide Array Sequence Analysis , Phorbol Esters/pharmacology , TNF-Related Apoptosis-Inducing Ligand , Tumor Cells, Cultured/cytology , Tumor Cells, Cultured/drug effects , Tumor Cells, Cultured/enzymology , Tumor Necrosis Factor-alpha/pharmacology
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