15 research outputs found
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Quality of diagnostic staging in patients with bladder cancer: A processâoutcomes link
BackgroundMuscle sampling is often used as a surrogate for staging quality in patients with bladder cancer. The association of staging quality at diagnosis and survival was examined among patients with bladder cancer.MethodsThe clinical records of all individuals within the Los Angeles Surveillance, Epidemiology, and End Results registry with an incident diagnosis of non-muscle-invasive bladder cancer in 2004-2005 were reviewed. Patient demographics, tumor characteristics, staging quality (presence of muscle in the specimen and mention of muscle in the pathology report), and vital status were recorded. With mixed-effects and competing-risks regression analyses, the association of patient and tumor characteristics with staging quality and cancer-specific survival was quantified.ResultsThe sample included 1865 patients, 335 urologists, and 27 pathologists. Muscle was reported to be present in 972 (52.1%), was reported to be absent in 564 (30.2%), and was not mentioned in 329 (17.7%) of the initial pathology reports. The presence of muscle did not differ according to the grade or depth of invasion. Mortality was associated with staging quality (Pâ<â.05). Among patients with high-grade disease, the 5-year cancer-specific mortality rates were 7.6%, 12.1%, and 18.8% when muscle was present, absent, and not mentioned, respectively.ConclusionsThe omission of muscle in the specimen or its mention in the pathology report in nearly half of all diagnostic resections was associated with increased mortality, particularly in patients with high-grade disease. Because urologists cannot reliably discern between high- and low-grade or Ta and T1 disease, it is contended that patients with bladder cancer should undergo adequate muscle sampling at the time of endoscopic resection
Respiratory virus-induced EGFR activation suppresses IRF1-dependent Interferon-λ and antiviral defense in airway epithelium
Viruses suppress host responses to increase infection, and understanding these mechanisms has provided insights into cellular signaling and led to novel therapies. Many viruses (e.g., Influenza virus, Rhinovirus [RV], Cytomegalovirus, Epstein-Barr virus, and Hepatitis C virus) activate epithelial epidermal growth factor receptor (EGFR), a tyrosine kinase receptor, but the role of EGFR in viral pathogenesis is not clear. Interferon (IFN) signaling is a critical innate antiviral host response and recent experiments have implicated IFN-λ, a type III IFN, as the most significant IFN for mucosal antiviral immune responses. Despite the importance of IFN-λ in epithelial antiviral responses, the role and mechanisms of epithelial IFN-λ signaling have not been fully elucidated. We report that respiratory virus-induced EGFR activation suppresses endogenous airway epithelial antiviral signaling. We found that Influenza virusâ and RV-induced EGFR activation suppressed IFN regulatory factor (IRF) 1âinduced IFN-λ production and increased viral infection. In addition, inhibition of EGFR during viral infection augmented IRF1 and IFN-λ, which resulted in decreased viral titers in vitro and in vivo. These findings describe a novel mechanism that viruses use to suppress endogenous antiviral defenses, and provide potential targets for future therapies
Quality of transurethral resection in patients with bladder cancer: A process-outcomes link.
EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production.
Airway epithelial cells are the primary cell type involved in respiratory viral infection. Upon infection, airway epithelium plays a critical role in host defense against viral infection by contributing to innate and adaptive immune responses. Influenza A virus, rhinovirus, and respiratory syncytial virus (RSV) represent a broad range of human viral pathogens that cause viral pneumonia and induce exacerbations of asthma and chronic obstructive pulmonary disease. These respiratory viruses induce airway epithelial production of IL-8, which involves epidermal growth factor receptor (EGFR) activation. EGFR activation involves an integrated signaling pathway that includes NADPH oxidase activation of metalloproteinase, and EGFR proligand release that activates EGFR. Because respiratory viruses have been shown to activate EGFR via this signaling pathway in airway epithelium, we investigated the effect of virus-induced EGFR activation on airway epithelial antiviral responses. CXCL10, a chemokine produced by airway epithelial cells in response to respiratory viral infection, contributes to the recruitment of lymphocytes to target and kill virus-infected cells. While respiratory viruses activate EGFR, the interaction between CXCL10 and EGFR signaling pathways is unclear, and the potential for EGFR signaling to suppress CXCL10 has not been explored. Here, we report that respiratory virus-induced EGFR activation suppresses CXCL10 production. We found that influenza virus-, rhinovirus-, and RSV-induced EGFR activation suppressed IFN regulatory factor (IRF) 1-dependent CXCL10 production. In addition, inhibition of EGFR during viral infection augmented IRF1 and CXCL10. These findings describe a novel mechanism that viruses use to suppress endogenous antiviral defenses, and provide potential targets for future therapies
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Plexus 2013
PLEXUS is a student organized publication that showcases artwork by UCI School of Medicine students, physicians, faculty, staff, and patients. True to its name, PLEXUS aspires to connect both healers and healing alike through the unifying language of art. This year, we have renewed our efforts to bring PLEXUS to the greater UCI community with improved distribution as well as outreach events, including a collaboration with the Bowers Art Museum. We would like to give a special thanks to our faculty advisor, Dr. Johanna Shapiro, and Dr. Ellena Peterson, Associate Dean of Admissions and Outreach. This book would not have been possible without their support.We hope you enjoy PLEXUS 2013.To contribute to PLEXUS, please send artwork to plexusjournal@ gmail.com. We look forward to seeing your submissions!Editors In Chief: Christine Lee, Hanna LiuCreative Writing: Jacqueline Kurth, Lorianne BurnsVisual Arts: Adam TruongLayout And Design: Nabila Haque, Esther JunAudio: Jessica Galant, Melody BesharatiMarketing And Outreach: Avinash Chaurasi
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EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production.
Airway epithelial cells are the primary cell type involved in respiratory viral infection. Upon infection, airway epithelium plays a critical role in host defense against viral infection by contributing to innate and adaptive immune responses. Influenza A virus, rhinovirus, and respiratory syncytial virus (RSV) represent a broad range of human viral pathogens that cause viral pneumonia and induce exacerbations of asthma and chronic obstructive pulmonary disease. These respiratory viruses induce airway epithelial production of IL-8, which involves epidermal growth factor receptor (EGFR) activation. EGFR activation involves an integrated signaling pathway that includes NADPH oxidase activation of metalloproteinase, and EGFR proligand release that activates EGFR. Because respiratory viruses have been shown to activate EGFR via this signaling pathway in airway epithelium, we investigated the effect of virus-induced EGFR activation on airway epithelial antiviral responses. CXCL10, a chemokine produced by airway epithelial cells in response to respiratory viral infection, contributes to the recruitment of lymphocytes to target and kill virus-infected cells. While respiratory viruses activate EGFR, the interaction between CXCL10 and EGFR signaling pathways is unclear, and the potential for EGFR signaling to suppress CXCL10 has not been explored. Here, we report that respiratory virus-induced EGFR activation suppresses CXCL10 production. We found that influenza virus-, rhinovirus-, and RSV-induced EGFR activation suppressed IFN regulatory factor (IRF) 1-dependent CXCL10 production. In addition, inhibition of EGFR during viral infection augmented IRF1 and CXCL10. These findings describe a novel mechanism that viruses use to suppress endogenous antiviral defenses, and provide potential targets for future therapies
EGFR activation suppresses respiratory virus-induced IRF1-dependent CXCL10 production
Airway epithelial cells are the primary cell type involved in respiratory viral infection. Upon infection, airway epithelium plays a critical role in host defense against viral infection by contributing to innate and adaptive immune responses. Influenza A virus, rhinovirus, and respiratory syncytial virus (RSV) represent a broad range of human viral pathogens that cause viral pneumonia and induce exacerbations of asthma and chronic obstructive pulmonary disease. These respiratory viruses induce airway epithelial production of IL-8, which involves epidermal growth factor receptor (EGFR) activation. EGFR activation involves an integrated signaling pathway that includes NADPH oxidase activation of metalloproteinase, and EGFR proligand release that activates EGFR. Because respiratory viruses have been shown to activate EGFR via this signaling pathway in airway epithelium, we investigated the effect of virus-induced EGFR activation on airway epithelial antiviral responses. CXCL10, a chemokine produced by airway epithelial cells in response to respiratory viral infection, contributes to the recruitment of lymphocytes to target and kill virus-infected cells. While respiratory viruses activate EGFR, the interaction between CXCL10 and EGFR signaling pathways is unclear, and the potential for EGFR signaling to suppress CXCL10 has not been explored. Here, we report that respiratory virus-induced EGFR activation suppresses CXCL10 production. We found that influenza virus-, rhinovirus-, and RSV-induced EGFR activation suppressed IFN regulatory factor (IRF) 1-dependent CXCL10 production. In addition, inhibition of EGFR during viral infection augmented IRF1 and CXCL10. These findings describe a novel mechanism that viruses use to suppress endogenous antiviral defenses, and provide potential targets for future therapies
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A Novel Video-Based Patient Education Program to Reduce Penile Prosthetic Surgery Cancellations
Penile prosthetic surgery is an effective treatment for men with erectile dysfunction. Cancellation of surgery is disruptive and costly to patients, physicians, and the healthcare system. This pilot study sought to analyze surgery cancellations and implement a video-based patient education program to decrease surgery noncompletion. Baseline penile prosthetic surgery completion, rescheduling, and cancellation rates among consecutively scheduled surgeries were determined using a national cohort. Selected prosthetic surgeons then implemented Vidscrip, a video-based patient education program. Prerecorded videos were delivered via text message 14 days, 7 days, and 1 day preoperatively, as well as 1 day postoperatively. Subsequent analysis determined noncompletion rates, reasons for noncompletion, surgeon volume, and video utilization. Two-hundred twenty-six surgeries were scheduled in the baseline cohort; 141 were completed, and 85 were rescheduled or canceled. Among the intervention cohort, 290 patients completed, 7 rescheduled, and 37 canceled surgery. After program implementation, the surgery noncompletion rate was reduced compared to baseline (13.2% vs. 37.6%, p 20 cases vs. â€20 cases: 8.20% vs. 32.0%, p = .35). Video utilization was widely variable among practices (median viewing time 58.6 min, IQR 5.09â113). Penile prosthetic surgery is frequently rescheduled or canceled. Implementing a video-based patient education program reduces surgery noncompletion, improving efficiency and quality of care. Wider implementation is needed to validate these findings, while cost-effectiveness analyses may further support their broad adoption
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