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1.
Int Forum Allergy Rhinol ; 7(6): 570-575, 2017 06.
Article in English | MEDLINE | ID: mdl-28296272

ABSTRACT

BACKGROUND: Ergonomics is the methodologic study of people's efficiency in their work environment and is based on anatomy, physiology, psychology, and engineering. Although highly studied in other work environments, little attention has been paid to surgeons until the landmark survey by Park et al in 2010. Many unique aspects of endoscopic surgery amplify task-related physical discomfort, and, because of these issues, we aimed to study the physical fatigue effects of functional endoscopic sinus surgery (FESS) performed in the standing and sitting positions. METHODS: Bilateral FESS was performed in 8 cadaver heads (4 in the standing position, 4 in the sitting position), following established ergonomic principles. Physical fatigue was assessed using a 27-point physical discomfort questionnaire, surface electromyography (EMG), and the NASA Task Load Index Survey. Paired and unpaired t tests were used for statistical analysis. RESULTS: Physical fatigue was noted after FESS performed in both positions. An overall similar task burden was seen when comparing the 2 positions, although the sitting position was more "frustrating" (p < 0.05). Discomfort after FESS in the standing position was worse in the legs and low back, whereas, in the sitting position, it was seen predominantly in the upper back and arms (p < 0.05). Mean power frequency EMG measurements demonstrated fatigue of major muscle groups in both positions. CONCLUSION: Significant physical fatigue is reported after a single FESS operation, with measurable EMG changes. Surgeons should be aware of the short- and long-term physical implications of their daily tasks, and should use this information to be proactive in decision-making for their longevity.


Subject(s)
Endoscopy , Nasal Surgical Procedures , Posture , Surgeons , Electromyography , Ergonomics , Fatigue/physiopathology , Humans , Male , Muscle, Skeletal/physiology
2.
Ann Otol Rhinol Laryngol ; 126(3): 224-228, 2017 Mar.
Article in English | MEDLINE | ID: mdl-28061548

ABSTRACT

OBJECTIVE: To determine if suprafascial harvest of the radial forearm free flap improves postoperative donor site outcomes compared to subfascial harvest. METHODS: Retrospective chart review. RESULTS: Forty-six patients underwent reconstruction of a head and neck defect with a radial forearm free flap (RFFF). Subfascial harvest of the RFFF was performed in 25 (53%) patients and suprafascial harvest performed in 22 (47%) patients. All donor sites were covered with a split thickness skin graft and a bolster that remained in place for 6 days. Postoperative tendon exposure at the donor site occurred in 5 (20%) of the patients in the subfascial group and in 0 (0%) of the patients in the suprafascial group ( P = .05; Fisher's exact test). Average tourniquet time was 117 minutes in the subfascial group and 102 minutes in the suprafascial group. Hematoma formation occurred at the donor site in 2 (8%) and 1 (5%) patients in the subfascial and suprafascial groups, respectively. There were no complete or partial flap losses in either group. CONCLUSIONS: Suprafascial harvest of the RFFF decreases the risk of postoperative tendon exposure. The suprafascial harvest technique does not increase harvest time or donor site complications, nor does it negatively impact flap vascularity.


Subject(s)
Dissection/methods , Fasciotomy/methods , Free Tissue Flaps , Postoperative Complications/prevention & control , Tendons , Tissue and Organ Harvesting/methods , Dissection/adverse effects , Fasciotomy/adverse effects , Female , Forearm , Humans , Male , Middle Aged , Postoperative Complications/etiology , Postoperative Complications/pathology , Plastic Surgery Procedures , Retrospective Studies , Skin Transplantation , Tissue and Organ Harvesting/adverse effects , Treatment Outcome , Wound Healing
3.
Laryngoscope ; 124(9): 2114-7, 2014 Sep.
Article in English | MEDLINE | ID: mdl-24577997

ABSTRACT

OBJECTIVES/HYPOTHESIS: There are numerous techniques for awake laryngeal injection, each with its limitations and technical challenges. We demonstrate a modification to the thyrohyoid approach for injection that stabilizes needle introduction and allows for consistent placement in a wide variety of larynges. STUDY DESIGN: Retrospective review at a tertiary care institution. METHODS: A retrospective review was performed of the charts for patients consecutively undergoing awake vocal fold injection laryngoplasty in 2013 for glottic insufficiency due to unilateral vocal fold paralysis, vocal fold atrophy, or sulcus vocalis using the laryngeal introducer technique. The consistency of needle placement, ease of technique, and patient tolerance was assessed. The technique utilizes a curved 1.5-inch 18-gauge needle as a laryngeal introducer through the thyroid notch. Laryngeal injection augmentation is then performed using a curved 3.5-inch 25-gauge spinal needle through the introducer. RESULTS: Twenty-one patients were identified who underwent awake vocal fold injection laryngoplasty for glottic insufficiency. All 21 injections were successfully placed. Five of seven injections attempted by resident physicians were able to be completed without attending assistance. Patient experience data demonstrated good tolerance, with a preference for the awake procedure as compared to that performed under general anesthesia. CONCLUSIONS: The laryngeal introducer technique is a novel way of performing awake laryngeal injections. It provides a high rate of success, the ability to be consistently performed by inexperienced clinicians, and is well tolerated by patients.


Subject(s)
Laryngoplasty/instrumentation , Laryngoplasty/methods , Vocal Cords , Adult , Aged , Equipment Design , Feasibility Studies , Female , Humans , Injections , Male , Middle Aged , Needles , Office Visits , Retrospective Studies , Young Adult
4.
Pancreas ; 38(4): 409-15, 2009 May.
Article in English | MEDLINE | ID: mdl-19142175

ABSTRACT

OBJECTIVES: The aim of the study was to evaluate the effect of combination therapy of apigenin and gemcitabine on cell proliferation, the cell cycle, and gemcitabine resistance in human pancreatic cancer cells. METHODS: Cell counting was used to assess the effect of single-agent and combination treatment on the proliferation of CD18 and AsPC-1 pancreatic cancer cells. Flow cytometry was performed to assess the effect of combination treatment on cell cycle progression and induction of apoptosis. Western blot analysis was used to evaluate phosporylated AKT (pAkt) and cell cycle proteins. The effect of apigenin on gemcitabine-resistant AsPC-1 cells was assessed via thymidine incorporation. RESULTS: Apigenin in combination with gemcitabine inhibited pancreatic cancer cell proliferation more than either agent alone. Combination treatment induced both S and G2/M phase arrest and increased apoptosis. Apigenin down-regulated pAkt expression and abrogated gemcitabine-mediated pAkt induction. In gemcitabine-resistant AsPC-1 cells, apigenin significantly inhibited cell proliferation in a dose-dependent manner. CONCLUSION: Combination treatment with apigenin and gemcitabine inhibited pancreatic cancer cell growth via cell cycle arrest, down-regulation of the prosurvival factor pAkt, and induction of apoptosis. Combination therapy may prove useful for the treatment of pancreatic cancer.


Subject(s)
Apigenin/pharmacology , Cell Proliferation/drug effects , Deoxycytidine/analogs & derivatives , Drug Resistance, Neoplasm/drug effects , Antimetabolites, Antineoplastic/pharmacology , Apoptosis/drug effects , Blotting, Western , Cell Cycle/drug effects , Cell Cycle Proteins/metabolism , Cell Line, Tumor , Deoxycytidine/pharmacology , Dose-Response Relationship, Drug , Drug Synergism , Flow Cytometry , G2 Phase/drug effects , Humans , Mitosis/drug effects , Pancreatic Neoplasms/metabolism , Pancreatic Neoplasms/pathology , Phosphorylation/drug effects , Proto-Oncogene Proteins c-akt/metabolism , S Phase/drug effects , Gemcitabine
5.
Pancreas ; 37(4): 426-31, 2008 Nov.
Article in English | MEDLINE | ID: mdl-18953257

ABSTRACT

OBJECTIVES: The antiproliferative mechanisms of flavonoid drugs inpancreatic cancer cells remain unclear. In this study, we evaluated the effects of the flavonoid apigenin on glucose uptake, on the expression of the glucose transporter 1 (GLUT-1), and on the phosphoinositide 3-kinase (PI3K)/Akt pathway in human pancreatic cancer cells. METHODS: Human pancreatic cancer cells were treated with apigenin and then underwent glucose uptake assays. Real-time reverse transcription-polymerase chain reaction and Western blot analysis were conducted to evaluate GLUT-1 and pAkt expression in CD18 and S2-013 human pancreatic cancer cells after treatment with apigenin or PI3K inhibitors (LY294002 and wortmannin). RESULTS: Apigenin (0-100 microM) significantly inhibited, in a dose-dependent fashion, glucose uptake in CD18 and S2-013 human pancreatic cancer cell lines. Apigenin inhibited both GLUT-1 mRNA and protein expression in a concentration- and time-dependent fashion. The PI3K inhibitors, like apigenin, downregulated both GLUT-1 mRNA and protein expression. CONCLUSIONS: Our results demonstrate that the flavonoid apigenin decreases glucose uptake and downregulates the GLUT-1 glucose transporter in human pancreatic cancer cells. In addition, the inhibitory effects of apigenin and the PI3K inhibitors on GLUT-1 are similar, indicating that the PI3K/Akt pathway is involved in mediating apigenin's effects on downstream targets such as GLUT-1.


Subject(s)
Adaptor Proteins, Signal Transducing/antagonists & inhibitors , Antineoplastic Agents/pharmacology , Apigenin/pharmacology , Apoptosis Regulatory Proteins/antagonists & inhibitors , Glucose Transporter Type 1/antagonists & inhibitors , Pancreatic Neoplasms/enzymology , Phosphoinositide-3 Kinase Inhibitors , Protein Kinase Inhibitors/pharmacology , Signal Transduction/drug effects , Adaptor Proteins, Signal Transducing/metabolism , Apoptosis Regulatory Proteins/metabolism , Cell Line, Tumor , Dose-Response Relationship, Drug , Glucose Transporter Type 1/genetics , Glucose Transporter Type 1/metabolism , Humans , Pancreatic Neoplasms/pathology , Phosphatidylinositol 3-Kinases/metabolism , RNA, Messenger/metabolism , Time Factors
6.
Mol Carcinog ; 47(11): 835-44, 2008 Nov.
Article in English | MEDLINE | ID: mdl-18404646

ABSTRACT

Pancreatic adeniocarcinoma is among the deadliest of human cancers. Apigenin, an antitumor flavonoid, inhibits pancreatic cancer cell proliferation in vitro. Geminin is a recently identified novel protein that plays a critical role in preventing abnormal DNA replication by binding to and inhibiting the essential replication factor Cdt1. Microarray analysis identified geminin to be downregulated in pancreatic cancer cells treated with apigenin. Therefore, we investigated the effects of apigenin on geminin expression and other proteins involved in replication (Cdc6, Cdt1, and MCM7) in pancreatic cancer cell lines CD18 and S2013. Real time RT-PCR and western blotting analysis showed that geminin expression is downregulated by apigenin at both mRNA and protein levels. Furthermore, treatment of cells with proteosome inhibitor MG132 reversed the downregulation of geminin by apigenin, supporting our hypothesis that the degradation pathway is another mechanism by which apigenin affects geminin expression. Apigenin treatment also resulted in downregulation of Cdc6 at both mRNA and protein levels. However, Cdt1 and MCM7 expression was not affected in apigenin-treated cells. The effect of apigenin treatment on geminin promoter activity was measured by transient transfection of Hela cells with a reporter gene, demonstrating that apigenin inhibited geminin promoter activity. Geminin expression was also evaluated in human pancreatic tissue (n = 15) by immunohistochemistry and showed that geminin is overexpressed in human pancreatic cancer compared to normal adjacent pancreatic tissue. In conclusion, our studies demonstrated that geminin is overexpressed in human pancreatic cancer and downregulated by apigenin which may contribute to the antitumor effect of this natural flavonoid.


Subject(s)
Apigenin/pharmacology , Biological Products/pharmacology , Cell Cycle Proteins/metabolism , Down-Regulation/drug effects , Gene Expression Regulation, Neoplastic/drug effects , Pancreatic Neoplasms/metabolism , Cell Cycle Proteins/genetics , Cell Line, Tumor , Geminin , Humans , Leupeptins/pharmacology , Nuclear Proteins/genetics , Nuclear Proteins/metabolism , Pancreatic Neoplasms/genetics , Pancreatic Neoplasms/pathology , Promoter Regions, Genetic/genetics , Proteasome Endopeptidase Complex/metabolism , Proteasome Inhibitors , RNA, Messenger/genetics
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