Average outpouring velocity and flow rate of grains discharged from a tilted quasi-2D silo

The flow of granular materials through constricted openings is important in many natural and industrial processes. These complex flows - featuring dense, dissipative flow in the bulk but low-dissipation, low density outpouring in the vicinity of the orifice - have long been characterized empirically by the Beverloo rule and, recently, modeled successfully using energy balance. The dependence of flow rate on the silo's angle with respect to gravity, however, is not captured by current models. We experimentally investigate the role of tilt angle in this work using a quasi-2D monolayer of grains in a silo. We measure mass flow rate, the average exit velocities of grains, and the packing fraction along the orifice with varying tilt angles. We propose a model that describes our results (and earlier findings with 3D systems [H. G. Sheldon and D. J. Durian, Granul. Matter 12, 579 (2010)]) by considering the dependence of outpouring speed and angle with respect to the orifice angle and, importantly, the angle of stagnant zones adjacent to the orifice. We conclude by posing questions about possible extensions of our model in order to describe spatial variations of exit velocity and density along the orifice cross section.Comment: 10 pages and 11 figure

Fluorescence Bronchoscopic Surveillance in Patients With a History of Non-Small Cell Lung Cancer

Background Second lung primaries occur at a rate of 2% per patient per year after curative resection for non-small cell lung carcinoma (NSCLC). The aim of this study was to evaluate the role of fluorescence bronchoscopy using the Xillix® LIFE-Lung Fluorescent Endoscopy SystemTM (LIFE-Lung system) in the surveillance of patients for second NSCLC primaries after resection or curative photodynamic therapy (PDT)

Impact of tumor size on outcomes after anatomic lung resection for stage 1A non–small cell lung cancer based on the current staging system

ObjectiveAnatomic segmentectomy may achieve results comparable to lobectomy for early-stage non–small cell lung cancer. The 7th edition of the AJCC Cancer Staging Handbook stratified the previous T1 tumor designation into T1a and T1b subsets, which still define stage 1A node-negative non–small cell lung cancer. We are left to hypothesize whether this classification may aid in directing the extent of surgical resection. We retrospectively reviewed our anatomic segmentectomy and lobectomy management of stage 1A non–small cell lung cancer to determine differences in survival and local recurrence rates based on the new stratification.MethodsWe performed a retrospective review of 429 patients undergoing resection of pathologically confirmed stage 1A non–small cell lung cancer via lobectomy or anatomic segmentectomy. Primary outcome variables included mortality, recurrence, and survival. Recurrence-free and cancer-specific survivals were estimated using the Kaplan–Meier method.ResultsPatients undergoing segmentectomy were older than patients undergoing lobectomy (mean age 69.2 vs 66.8 years, P < .006). The mean preoperative forced expiratory volume in 1 second was significantly lower in the segmentectomy group than in the lobectomy group (71.8% vs 81.1%, P = .02). Mortality was similar after segmentectomy (1.1%) and lobectomy (1.2%). There was no difference in mortality, recurrence rates (14.0% vs 14.7%, P = 1.00), or 5-year cancer-specific survival (T1a: 90% vs 91%, P = .984; T1b: 82% vs 78%, P = .892) when comparing segmentectomy and lobectomy for pathologic stage 1A non–small cell lung cancer, when stratified by T stage.ConclusionsAnatomic segmentectomy may achieve equivalent recurrence and survival compared with lobectomy for patients with stage 1A non–small cell lung cancer. Prospective studies will be necessary to delineate the potential merits of anatomic segmentectomy in this setting

Anatomic segmentectomy for stage I non–small-cell lung cancer: Comparison of video-assisted thoracic surgery versus open approach

ObjectivesAnatomic segmentectomy is increasingly being considered as a means of achieving an R0 resection for peripheral, small, stage I non–small-cell lung cancer. In the current study, we compare the results of video-assisted thoracic surgery (n = 104) versus open (n = 121) segmentectomy in the treatment of stage I non–small-cell lung cancer.MethodsA total of 225 consecutive anatomic segmentectomies were performed for stage IA (n = 138) or IB (n = 87) non–small-cell lung cancer from 2002 to 2007. Primary outcome variables included hospital course, complications, mortality, recurrence, and survival. Statistical comparisons were performed utilizing the t test and Fisher exact test. The probability of overall and recurrence-free survival was estimated with the Kaplan-Meier method, with significance being estimated by the log-rank test.ResultsMean age (69.9 years) and gender distribution were similar between the video-assisted thoracic surgery and open groups. Average tumor size was 2.3 cm (2.1 cm video-assisted thoracic surgery; 2.4 cm open). Mean follow-up was 16.2 (video-assisted thoracic surgery) and 28.2 (open) months. There were 2 perioperative deaths (2/225; 0.9%), both in the open group. Video-assisted thoracic surgery segmentectomy was associated with decreased length of stay (5 vs 7 days, P < .001) and pulmonary complications (15.4% vs 29.8%, P = .012) compared with open segmentectomy. Overall mortality, complications, local and systemic recurrence, and survival were similar between video-assisted thoracic surgery and open segmentectomy groups.ConclusionsVideo-assisted thoracic surgery segmentectomy can be performed with acceptable morbidity, mortality, recurrence, and survival. The video-assisted thoracic surgery approach affords a shorter length of stay and fewer postoperative pulmonary complications compared with open techniques. The potential benefits and limitations of segmentectomy will need to be further evaluated by prospective, randomized trials

F-box protein complex FBXL19 regulates TGFβ1-induced E-cadherin down-regulation by mediating Rac3 ubiquitination and degradation

Background: Rac3 is a small GTPase multifunctional protein that regulates cell adhesion, migration, and differentiation. It has been considered as an oncogene in breast cancer; however, its role in esophageal cancer and the regulation of its stability have not been studied. F-box proteins are major subunits within the Skp1-Cullin-1-F-box (SCF) E3 ubiquitin ligases that recognize particular substrates for ubiquitination and proteasomal degradation. Recently, we have shown that SCFFBXL19 targets Rac1 and RhoA, thus regulating Rac1 and RhoA ubiquitination and degradation. Here, we demonstrate the role of FBXL19 in the regulation of Rac3 site-specific ubiquitination and stability. Expression of TGFβ1 is associated with poor prognosis of esophageal cancer. TGFβ1 reduces tumor suppressor, E-cadherin, expression in various epithelial-derived cancers. Here we investigate the role of FBXL19-mediated Rac3 degradation in TGFβ1-induced E-cadherin down-regulation in esophageal cancer cells.Methods: FBXL19-regulated endogenous and over-expressed Rac3 stability were determined by immunoblotting and co-immunoprecipitation. Esophageal cancer cells (OE19 and OE33) were used to investigate TGFβ1-induced E-cadherin down-regulation by Immunoblotting and Immunostaining.Results: Overexpression of FBXL19 decreased endogenous and over-expressed Rac3 expression by interacting and polyubiquitinating Rac3, while down-regulation of FBXL19 suppressed Rac3 degradation. Lysine166 within Rac3 was identified as an ubiquitination acceptor site. The FBXL19 variant with truncation at the N-terminus resulted in an increase in Rac3 degradation; however, the FBXL19 variant with truncation at the C-terminus lost its ability to interact with Rac3 and ubiquitinate Rac3 protein. Further, we found that Rac3 plays a critical role in TGFβ1-induced E-cadherin down-regulation in esophageal cancer cells. Over-expression of FBXL19 attenuated TGFβ1-induced E-cadherin down-regulation and esophageal cancer cells elongation phenotype.Conclusions: Collectively these data unveil that FBXL19 functions as an antagonist of Rac3 by regulating its stability and regulates the TGFβ1-induced E-cadherin down-regulation. This study will provide a new potential therapeutic strategy to regulate TGFβ1 signaling, thus suppressing esophageal tumorigenesis. © 2014 Dong et al.; licensee BioMed Central Ltd