Introduction: We sought to assess the accuracy of using stone volume (SV) estimated with a software algorithm as a predictor for stone passage in a trial of medical expulsive therapy (MET). Methods: We identified patients with ureteral stones discharged from the ER on MET. Patients with infection, non-ureteral stones, or needing immediate surgical intervention were excluded. For each stone, longest dimension (LD) was recorded and SV was estimated by a computed tomography (CT)-based region growing (RG) algorithm and standard ellipsoid formula (EF). Stone passage within 30 days was assessed via electronic chart and followup phone call. Results: Fifty-one patients were included for analysis (53±16.7 years, 24% female). The mean LD was 4.85±2.02 mm. The mean SV was similar by EF and RG (0.051±0.057cm3 vs. 0.049± 0.052 cm3; p=0.28). Thirty-three (65%) patients passed their stone, while 18 (35%) did not. The mean LD for passed stones vs. failed passage was 4.1±1.7 mm vs. 6.2±1.8 mm (p=0.0002); the mean EF volume was 0.028±0.035 cm3 vs. 0.093±0.066 cm3 (p=0.00007); and the mean volume by RG was 0.028±0.027cm3 vs. 0.088±0.063 cm3 (p=0.00005). Conclusions: The clinical utility of using SV estimated by software algorithm as a predictor for success of MET has not previously been examined. We demonstrate that spontaneously passed stones had a significantly smaller volume than those requiring intervention. Further prospective studies are needed to validate these findings and establish volume thresholds for probability of stone passage.
Introduction: This study sought to characterize delays and estimate resulting costs during nephrolithiasis surgery. Methods: Independent observers documented delays during ureteroscopy (URS) and percutaneous nephrolithotomy (PCNL) procedures. Fifty index cases over a period of three months was considered sufficient to observe the generalizable trends. Operating room staff, excluding the surgeons, were blinded. Time-related metrics and delays preventing case progression were recorded using a smartphone-accessible data collection instrument. Delays were categorized as: 1) missing equipment; 2) missing personnel; 3) equipment malfunction; or 4) delay due to case complexity. The first two categories were regarded as preventable and the latter two non-preventable. Results: Forty URS and 18 PCNL cases were included. There was a total of 56 delays in 35 (65%) cases. Twelve (67%) PCNLs and 23 (58%) URSs had delays (p=0.57). The mean cumulative delay per case was 3.5±3.2 minutes. Pre-start delays (n=17) were 4.5±3.5 minutes on average while intraoperative delays (n=39) were 3.1±2.9 minutes (p=0.167). Delays were evenly spread among the four categories. Thirty-one (55%) delays were preventable (mean 3.7±3.2 minutes) while 25 (45%) were non-preventable (mean 3.2±3.2 minutes) (p=0.58). This translates to $137 per case in preventable costs. Conclusions: Preventable operative delays are encountered frequently in nephrolithiasis surgery, translating to significant additional charges and costs. We demonstrate a rationale for the development of improved communication and workflow protocols to increase efficiency in endourological surgeries. Key limitations are the observational nature of the study and sample size.
Introduction: Although Candida spp. are associated with invasive candidiasis in immunocompromised hosts, rates of asymptomatic colonization with the fungus are high. Candida has been associated with a variety of cancers and is thought to play a role in carcinogenesis. Beta glucans are polysaccharide components of the fungal cell wall that are more highly expressed in the more invasive, hyphal form of Candida. Recent data suggests that EPHA2, a tyrosine kinase receptor on oral epithelial cells, acts as a pattern recognition receptor for beta-glucans. We tested the hypothesis that beta-glucans promote proliferation and/or migration of squamous cell carcinoma cells through interactions with EPHA2. Methods: W18 cells, with wild-type EPHA2 expression, were derived from murine squamous cell carcinoma cells induced by classical DMBA/TPA protocol. SCC-728 is a squamous cell carcinoma cell line from an EphA2 KO mouse. The SCC-728 cell line was also used to generate an EPHA2-reconstituted cell line. HIGK cells are an immortalized oral epithelial cell line. Cells were cultured in 6 well plates to confluence in DMEM at 37° Celsius. Plates were scratched using a 200-microliter pipette tip and treated. Microscopic images from 0 and 24 hours were compared and analyzed visually by ImageJ. Beta-glucan from Saccharomyces was tested at 12.5 micrograms/milliliter. EGF (20 nanograms/milliliter) was the positive control for cell proliferation. Mitomycin C (10micrograms/milliliter) was the negative control for proliferation. Other glucans tested include zymosan (12.5 micrograms/milliliter) and pullulans (12.5 micrograms/milliliter). Results In the presence of beta-glucan, wild-type SCC cells (p<0.05) and EPHA2-reconstitued cells showed significant closure compared to control. EPHA2-KO cells did not show significant closure compared to controls on exposure to beta-glucans. All cell lines showed significant closure on treatment with EGF. Treatment with mitomycin C, alone or in combination with EGF or beta-glucan, prevented significant closure in all cell lines. Significant closure was seen with zymosan- and pullulans-treated cells. Conclusion: SCC cells showed increased proliferation in the presence of beta-1,6-glucan and beta-1,3-glucan from Saccharomyces. SCC cells showed migration or proliferation in the presence of alpha-1,4- and alpha-1,6-glucan, but less significant than beta-1,6-glucan and beta-1,3-glucan. Beta-glucan can induce EphA2-dependent cell membrane retraction similar to its native ligands. Citation Format: Sara Maskal, Santosh Ghosh, Chad Zender, Jason Thuener, Aaron Weinberg. Fungal beta-glucans, EphA2, and oral cancer: Preliminary observations [abstract]. In: Proceedings of the AACR-AHNS Head and Neck Cancer Conference: Optimizing Survival and Quality of Life through Basic, Clinical, and Translational Research; 2019 Apr 29-30; Austin, TX. Philadelphia (PA): AACR; Clin Cancer Res 2020;26(12_Suppl_2):Abstract nr A33.
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