Thermal injury to common operating room materials by fiber optic light sources and endoscopes.

PURPOSE: To determine the thermal energy damage potential by heat sources, such as endoscopes and fiber optic light cables, in contact with materials commonly placed around an operating room (OR) table. MATERIALS AND METHOD: Injury by xenon and halogen light sources were tested by direct and indirect contact using fiber optic light bundle cables and scopes at light intensities between ranging from Standby to 100%. The scopes had diameters ranging from 2.7 mm to 10 mm and were set at varying angles. The materials tested were surgical drapes, cotton towels, child shirts, child pants, lap sponges, X-ray detectable sponges, and Mayo covers. The damage potential was determined qualitatively by presence of smoking or smell of burning. RESULTS: Permutations involving direct contact were able to cause thermal injury, while permutations involving indirect contact, endoscopes, or halogen lamp were not. The xenon light source with the fiber optic light cable created thermal injury at light intensities of 50%, 75%, and 100%. Time to injury increased as light intensity was decreased. Only the surgical drape, child shorts, and cotton towel showed evidence of burn injury. CONCLUSIONS: This report supports the potential for thermal injury to the patient secondary to fiber optic light sources, although this potential may be limited in extent. The injury risk can be reduced by avoiding direct contact to materials overlying the patient, confirming standby mode or 25% light intensity, and maintaining the endoscope connected to the fiber optic cable at all times.

Reinke's Edema.

Reinke's edema (RE) is the polypoid degeneration of one or both vocal folds within Reinke's space. The viscoelastic properties of the mucosal folds are characteristically altered by the expansion of the subepithelial space. Most frequently, patients present with dysphonia, with women being more affected than men. The primary risk factor is tobacco use. Voice overuse and laryngopharyngeal reflux are also considered to be contributory. Although RE shares the same primary risk factor as malignancy, the risk of malignancy is low, and dysplasia is found only in 0% to 3% of cases. Treatment is focused on decrease of risk factors, such as implementation of smoking cessation, voice therapy, and reflux control. Surgical techniques aim to decrease redundant polypoid mucosa in order to improve voice and restore the glottic airway. Recurrence of RE is high.

Honey as a Treatment in Otorhinolaryngology: A Review by Subspecialty.

OBJECTIVES: To provide an up-to-date review of honey's effectiveness and potential applications in otorhinolaryngology. METHODS: A literature search of the online databases PubMed, EMBASE, and Cochrane Central Register of Controlled Trials was conducted. RESULTS: Sixty-three studies were identified within head and neck surgery (n = 23, 36%); pediatric otolaryngology (n = 18, 29%); rhinology, sinus, and skull base surgery (n = 11, 17%); otology (n = 6, 10%), facial plastic and reconstructive surgery (n = 3, 5%); and laryngology (n = 2, 3%). Studies included 6 meta-analyses, 44 randomized control trials, 5 case reports, and 8 animal models or in vitro studies. Of 55 clinical studies, 50 reported Level 1 evidence (prospective randomized control trials), and 5 reported Level 4 evidence (case series). The evidence level by subspecialty was: head and neck surgery (Level 1 n = 23), pediatrics (Level 1 n = 18), rhinology (Level 1 n = 7, level 4 n = 1), otology (Level 1 n = 1, Level 4 n = 3), facial plastics and reconstructive surgery (Level 4 n = 1), and laryngology (Level 1 n = 2). CONCLUSIONS: Honey can be used for a variety of otolaryngology conditions. The highest quality meta-analyses support oral honey for prevention and treatment of oral mucositis in cancer patients, cough associated with upper respiratory infection in children, and pain control after tonsillectomy. Further research will likely justify broader applications.

Does Reinke's Edema Grade Determine Premalignant Potential?

OBJECTIVE: Reinke's edema (RE) is a benign disease of the vocal folds with a wide spectrum of clinical severity. We aim to evaluate the clinical impact of RE grade and determine if RE grade correlates with severity of dysplasia and tobacco exposure. METHODS: Patients with isolated RE who underwent surgical excision between December 2010 and December 2014 were retrospectively reviewed. The RE grade was determined from archived laryngeal videostroboscopy exams. Pathologic severity of dysplasia, categorized by squamous intraepithelial neoplasia (SIN) classification, and tobacco history were extracted from medical records. RESULTS: Of 95 lesions, 3 (3.16%) were RE grade 1, 33 (34.74%) were RE grade 2, 24 (25.26%) were RE grade 3, and 35 (36.84%) were RE grade 4. Fifty-nine lesions (62.11%) had no dysplasia (SIN0), 19 (20.00%) had mild dysplasia (SIN1), 15 (15.79%) had moderate dysplasia (SIN 2), and 2 (2.11%) had severe dysplasia (SIN3). The 2 patients with severe dysplasia had grade 4 lesions. No statistical correlation was identified between RE grade and the severity of dysplasia. Furthermore, no statistical correlation was seen between tobacco exposure and the severity of dysplasia or the RE grade. CONCLUSIONS: Size of RE lesion does not reflect premalignancy. The majority of RE lesions, regardless of size, have little to no premalignant potential. Severe dysplasia/carcinoma in situ may be more likely seen in grade 4 lesions; however, the paucity of severe dysplasia published in RE data and in this cohort preclude any formal inference. Further study of grade 4 lesions is warranted.

Oncologic benefit of tonsillectomy in stage I and II tonsil cancer: a surveillance epidemiology and end results database review.

IMPORTANCE: Treatment of low-stage tonsil cancer with radiotherapy is common, but the type of diagnostic procedure prior to radiotherapy varies. This study uses the Surveillance Epidemiology and End Results (SEER) registry to determine whether tonsillectomy or other surgical procedures prior to radiotherapy have an impact on outcome. OBJECTIVE: To demonstrate whether tonsillectomy adds oncologic advantage over biopsy alone in stage I or II tonsil cancers prior to definitive radiotherapy. DESIGN: Retrospective study of the SEER program. PARTICIPANTS: A total of 524 patients with stage I and II primary tonsil carcinoma diagnosed during the period 1988 through 2006 who received definitive radiation treatment. MAIN OUTCOMES AND MEASURES: Hazard ratios, 5-year disease-specific survival (DSS), 5-year overall survival (OS), and Kaplan-Meier survival curves. Subgroup univariate and multivariate analysis of survival compared the following variables: sex, T category (T1 vs T2), year of diagnosis (1988-2003 vs 2004-2006), and surgical status (preradiation tonsillectomy vs biopsy only). A log-rank test compared Kaplan-Meier survival analysis for the surgical status subgroups. RESULTS Statistically significant contributors to survival (DSS and OS) included age (P < .001, DSS), surgical status (P = .001, DSS), and year of diagnosis (P = .02, DSS). Treatment with radiation after tonsillectomy yielded a 5-year OS of 83% (95% CI, 77%-88%) and a 5-year DSS of 90% (95% CI, 84%-93%). This compares with an OS of 64% (95% CI, 54%-71%) and DSS of 76% (95% CI, 68%-82%) for radiation therapy after biopsy alone. CONCLUSIONS AND RELEVANCE: SEER data suggest that tonsil resection prior to radiation therapy is associated with improved survival in low-stage tonsil cancer. Although selection bias is a likely factor in this analysis, the effect remains after controlling for age and year of treatment.

The combination of 5-fluorouracil plus p53 pathway restoration is associated with depletion of p53-deficient or mutant p53-expressing putative colon cancer stem cells.

The cancer stem cell hypothesis suggests that rare populations of tumor-initiating cells may be resistant to therapy, lead to tumor relapse and contribute to poor prognosis for cancer patients. We previously demonstrated the feasibility of p53 pathway restoration in p53-deficient tumor cell populations using small molecules including ellipticine or its derivatives. We now establish a single cell p53-regulated green fluorescent protein (EGFP)-reporter system in human DLD1 colon tumor cells expressing mutant p53 protein. We use these p53-EGFP reporter DLD1 cells to investigate the status of p53 transcriptional activity in putative colon cancer stem cell populations following exposure to p53 pathway-restoring drugs and/or classical chemotherapy. We demonstrate induction of p53-specific EGFP reporter fluorescence following overexpression of p53 family member p73 by an Adenovirus vector. We further show that p53-reporter activity is induced in DLD1 putative cancer stem cell side-populations analyzed by their Hoechst dye efflux properties following treatment with the p53 pathway restoring drug ellipticine. Combination of ellipticine with the cytotoxic agent 5-fluorouracil resulted in increased cytotoxicity as compared to either agent alone and this was associated with depletion of putative cancer stem cell populations as compared with 5-FU alone treatment. Our results support the feasibility of therapeutic targeting of mutant p53 in putative cancer stem cells as well as the potential to enhance cytotoxic chemotherapy.

Effects of low confluency, serum starvation and hypoxia on the side population of cancer cell lines.

The cancer stem cell theory describes a small subset of cancer cells that have the ability to initiate and drive the growth of a tumor. The niche refers to the environmental factors and the surrounding cells within which the tumor develops. The exact relationship between cancer stem cells and the tumor niche is not known. However, using side population analysis by flow cytometry, it is possible to analyze the relationship between environmental stresses and putative cancer stem cells. The side population is a subpopulation of cells that efflux Hoechst 33342 and has been previously shown to be enriched for cancer stem cells. Using this technique, we characterized the response of side population cells to low confluency, serum starvation and hypoxia using three different human cancer cell lines. We found that these stresses, characteristic of the tumor niche enrich the side population of DLD1, SW480 and MCF7 cancer cell lines, thus possibly predisposing the tumor to a more malignant phenotype.

The effect of estradiol on in vivo tumorigenesis is modulated by the human epidermal growth factor receptor 2/phosphatidylinositol 3-kinase/Akt1 pathway.

To determine whether the epidermal growth factor receptor 2 (ErbB2) and Akt1 can alter the in vivo growth of MCF-7 cells, parental cells or cells stably transfected with constitutively active Akt1 (myr-Akt1) or dominant-negative Akt1 mutants (K179M-Akt1 and R25C-Akt1) were implanted into athymic nude mice. Tumor growth was monitored in the presence or absence of the antiestrogen tamoxifen and the selective ErbB2 inhibitor, AG825. MCF-7 [parental or empty vector transfected, cytomegalovirus (CMV)] and myr-Akt1 cells formed tumors upon estradiol supplementation after 20-30 d (59-, 29-, and 17-fold increase in tumor volume, respectively). Tamoxifen and AG825 blocked the estradiol effect by 93 and 96% in MCF-7 xenografts, 88 and 81% in CMV xenografts, and 91% in myr-Akt1 xenografts. Furthermore, AG825 suppressed the growth of established tumors in CMV and myr-Akt1 inoculated animals by 68 and 75%, respectively, as compared with continued estrogen supplementation, suggesting a role for ErbB2. When K179M-Akt1 or R25C-Akt1 cells were injected into ovariectomized animals, tumor growth was reduced upon estradiol treatment by 95% and 98%, respectively, supporting a role for Akt1. In contrast to ovariectomized animals, in intact animals, myr-Akt1 cells could establish tumors without estradiol priming after 40-50 d (20-fold increase in tumor volume). Loss of Akt1 phosphorylation was associated with tumor growth inhibition. Immunohistochemical assays showed that in tumors from parental and CMV xenografts, estradiol decreased estrogen receptor-alpha expression and induced progesterone receptor expression and Akt phosphorylation, effects that were inhibited by tamoxifen, AG825, and R25C-Akt1 by 89, 82, and 77% for progesterone receptor expression and 48, 66, and 73% for pAkt expression, respectively. Cumulatively, our results suggest that Akt1 and ErbB2 are involved in in vivo tumorigenesis and modulation of estrogen receptor-alpha expression and activity.