Introduction Artificial Intelligence (AI) platforms have gained widespread attention for their distinct ability to generate automated responses to various prompts. However, its role in assessing the quality and readability of a provided text remains unclear. Thus, the purpose of this study is to evaluate the proficiency of the conversational generative pre-trained transformer (ChatGPT) in utilizing the DISCERN tool to evaluate the quality of online content regarding shock wave therapy for erectile dysfunction. Methods Websites were generated using a Google search of “shock wave therapy for erectile dysfunction” with location filters disabled. Readability was analyzed using Readable software (Readable.com, Horsham, United Kingdom). Quality was assessed independently by three reviewers using the DISCERN tool. The same plain text files collected were inputted into ChatGPT to determine whether they produced comparable metrics for readability and quality. Results The study results revealed a notable disparity between ChatGPT's readability assessment and that obtained from a reliable tool, Readable.com (p<0.05). This indicates a lack of alignment between ChatGPT's algorithm and that of established tools, such as Readable.com. Similarly, the DISCERN score generated by ChatGPT differed significantly from the scores generated manually by human evaluators (p<0.05), suggesting that ChatGPT may not be capable of accurately identifying poor-quality information sources regarding shock wave therapy as a treatment for erectile dysfunction. Conclusion ChatGPT’s evaluation of the quality and readability of online text regarding shockwave therapy for erectile dysfunction differs from that of human raters and trusted tools. Therefore, ChatGPT's current capabilities were not sufficient for reliably assessing the quality and readability of textual content. Further research is needed to elucidate the role of AI in the objective evaluation of online medical content in other fields. Continued development in AI and incorporation of tools such as DISCERN into AI software may enhance the way patients navigate the web in search of high-quality medical content in the future.
Abstract Prostate cancer (PCa) is the most common non-cutaneous cancer among American men. In 2019, 174,650 new patients will be diagnosed from this disease. Most patients with localized PCa could be treated successfully. However, when PCa develops into castrate-resistant prostate cancer (CRPCa), the five-year survival rate drops below 30%. Neuroendocrine prostate cancer (NEPCa) is an aggressive subtype of PCa observed in 20%-30% CRPCa patients. Understanding how NEPCa progressed from prostate adenocarcinoma could reveal novel therapeutic targets. Previous studies indicate that activation of Wnt/beta-Catenin signaling promotes the progression to CRPCa with an increased NE differentiation. Additionally, animal studies suggest that Wnt/beta-Catenin signaling is active in NEPCa. Here we explored the mechanisms that promote Wnt/beta-Catenin signaling in NEPCa. Using TRAMP mice, which develop NEPCa after castration, we assessed the expression of Wnt-related genes and found that after androgen deprivation, the expression of Wnt7A is increased in prostate derived from both wild type and TRAMP mice but the expression of DKK1, a Wnt inhibitor, is decreased in wild type prostate but not in TRAMP prostate. The elevated expression of Wnt7a in combination with the lack of induction of Dkk1 in TRAMP tumors provides a mechanism to activate Wnt/beta-Catenin signaling in these tumors. Furthermore, we found the expression of YES-associated Protein (YAP1), a key transcriptional coactivator of Hippo pathway, is lost in NEPCa, in contrast to the elevated expression of YAP1 in high-grade prostate adenocarcinoma. YAP1 knockdown activated Wnt/beta-Catenin activity in PCa PC3 and 22Rv1 cells, indicating that the loss of YAP1 expression provides another mechanism to activate Wnt/beta-Catenin signaling, promoting NEPCa phenotype in PCa cells. Funding: This study is supported by: FWCC/Foundation Legacy Funds, DOD New Investigator Award, The Office of Research SEED awards, NIH R01 AND R03. Citation Format: Siyuan Cheng, Shu Yang, Nestor Prieto-Dominguez, Zachary M. Connelly, Yingli Shi, Xiuping Yu. Loss of YAP1 activates Wnt/beta-Catenin signaling in prostate cancer [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4861.
We report on the treatment of p53‐positive cancer cell lines with chemical inhibitors of transcription, translation and PI‐3 kinase‐like kinases (PIKKs). Our goal was to determine optimal concentrations of, and exposure times for, chemical inhibitor treatments. These experiments were prerequisite for our studies of the role nonsense‐mediated mRNA decay (NMD) plays in p53 expression. Cultured p53‐positive cancer cells were treated with varied concentrations of cycloheximide, caffeine, wortmannin, or actinomycin D to determine optimal concentrations. Cells were also treated with constant inhibitor concentrations in time‐course experiments to determine optimal duration of exposure. Treated cell samples were divided equally for protein and total RNA isolation. Protein samples were subjected to SDS‐PAGE and western analyses for p53 and beta‐actin. RNA samples were used to synthesize cDNA, which was subjected to TaqMan quantitative RT‐PCR (qRT‐PCR) analysis for p53 and beta‐actin. Western and qRT‐PCR data are consistent with optimal chemical inhibitor concentrations being substantially higher for HepG2 cells compared to MCF‐7 and HeLa. However, chemical inhibitor exposure times required to achieve optimal effect was not widely varied between cell lines studied. Through our determination of optimal conditions for chemical inhibition of transcription, translation and PIKK activity in p53‐positive cell lines, we conclude that cell lines studied require widely different concentrations of, but not different exposure times to, chemical inhibitors. Therefore, we determined optimal concentrations and exposure times for chemical inhibition in our studies of the role of NMD in p53 expression. Grant Funding Source : University of Tampa Chemistry, Biochemistry & Physics Departmental Student Research Support Fund
Abstract Prostate cancer (PCa) is the most common non-skin cancer and the 3rd leading cause of cancer-related death in American men. Androgen ablation therapy has been the gold standard for treating advanced stage PCa since the 1960s. Initially, the PCa patients respond to hormone ablation very positively. However, over time these tumors almost always become resistant to androgen ablation therapy, and tumors begin to grow again. Recent studies found after failure of the new drugs that block androgen action, PCa has increased neuroendocrine phenotype. Understanding the mechanisms through which PCa cells gain neuroendocrine phenotype is critical for the development of novel therapeutics. Polycomb repressive complex are involved in early embryo development and carcinogenesis in several types of cancer including PCa. In this study, we evaluated the involvement of Polycomb proteins in neuroendocrine PCa. Using immunohistochemistry staining, we examined the expression of Polycomb protein EZH2 in advanced stage PCa. We found that EZH2 is highly expressed in both human and mouse neuroendocrine PCa. Also, we found when PCa cells are induced to undergo neuroendocrine differentiation, multiple Polycomb genes are induced. These data suggest that Polycomb genes play a role in the development of neuroendocrine PCa. Citation Format: Zachary Connelly, Shu Yang, Anthony Blankenship, Xiuping Yu. Role of polycomb proteins in neuroendocrine prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1514.
Abstract Prostate cancer (PCa) is the most common non-skin cancer in American men. Each year, about 164,690 new patients will be diagnosed and about 29,430 men will die from this disease in 2018. Studies have identified several factors that increase the risk of PCa, including age, race, family history, and some diet factors. However, the exact cause of PCa remains unclear. Prostate is an androgen dependent organ and the growth of PCa also dependents on androgen and AR signaling. It is well established that AR signaling is the central player in promoting PCa progression. Here, we explore if AR signaling also plays a role in prostate carcinogenesis. We found that activation of AR signaling in normal prostate epithelial cells suppressed their cell proliferation in vitro but induced carcinogenesis in vivo. To explore the mechanisms that contribute to the differential effects of AR in vitro and in vivo, we examined if AR signaling induces genome instability in prostate epithelial cells, resulting in carcinogenesis and tumor progression. Senescence-associated beta-galactosidase staining results indicated that androgen treatment induced cellular senescence of prostate epithelial cells. Also, we found that the cells that survived the cellular senescence had altered genome ploidy and increased expression of active DNA-PK, suggesting that non-homologous end joining repair pathway is active in these cells. Our data support that AR signaling promotes genome instability in prostate epithelial cells, contributing to carcinogenesis. This may explain the high frequency of cancer developed in hormone-regulated organs such as prostate, mammary gland, and liver. Funding: This study was supported by: FWCC/Foundation Legacy Funds, DOD New Investigator Award, The Office of Research SEED awards, The Department of Biochemistry & Molecular Biology. Citation Format: Siyuan Cheng, Shu Yang, Zachary M. Connelly, Fenghua Chen, Xiuping Yu. AR signaling promotes prostate carcinogenesis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4302.
Prostate cancer (PCa) is the leading cancer among men. Androgen Deprivation Therapy (ADT) is a common treatment for advanced PCa. However, ADT eventually fails and PCa relapses, developing into castration-resistant prostate cancer (CRPCa). Although alternative pathways such as cancer stem-cell pathway and neuroendocrine differentiation bypass androgen receptor (AR) signaling, AR remains the central player in mediating CRPCa. In this study, we identified a mechanism that retains AR signaling after androgen deprivation. The TRAMP SV40 T antigen transgenic mouse is a model for PCa. The expression of SV40 T-antigen is driven by the androgen-responsive, prostate specific, Probasin promoter. It has been recognized that in this model, T-antigen is still expressed even after androgen ablation. It is unclear how the androgen-responsive Probasin promoter remains active and drives the expression of T-antigen in these tumors. In our study, we found that the expression of Foxa2, a forkhead transcription factor that is expressed in embryonic prostate and advanced stage prostate cancer, is co-expressed in T-antigen positive cells. To test if Foxa2 activates AR-responsive promoters and promotes the expression of T-antigen, we established the prostate epithelial cells that stably express Foxa2, NeoTag1/Foxa2 cells. Neotag1 cells were derived from the Probasin promoter driven SV40 T-antigen transgenic mouse. We found ectopic expression of Foxa2 drives the T-antigen expression regardless of the presence of androgens. Using this model system, we further explored the mechanism that activates AR-responsive promoters in the absence of androgens. Chromatin immunoprecipitation revealed the occupancy of both H3K27Ac, an epigenetic mark of an active transcription, and Foxa2 at the known AR target promoters, Probasin and FKBP5, in the absence of androgen stimulation. In conclusion, we have identified a mechanism that enables PCa to retain the AR signaling pathway after androgen ablation.
Ureteral stent placement is one of the most common procedures performed by urologists, and is typically done in the operating room. At Ochsner-LSU Health Shreveport, urologists have a unique setting allowing them to place ureteral stents for patients present in the outpatient ambulatory clinic without the need for nitrous oxide. This allows patients to avoid being admitted to the hospital and receiving subsequent general anesthesia in the operating room. Therefore, our novel study evaluates the feasibility, safety, and cost-effectiveness of ureteral stents insertion in the clinic.In this study, we analyzed 240 patients with a total of 279 different ureteral stent insertion encounters to evaluate the safety and costs of stenting in the clinic compared to the operating room. Stents were placed in the outpatient clinic for 126 patients, which required either a new ureteral stent insertion or a scheduled stent exchange.Overall, there was an increased age and length of stent duration among those who were stented in the clinic. We did not observe any increase in narcotics use, pain, adverse injuries, or differences in stent length. The total cost of a stent insertion operating room was $16,349.91 whereas the clinic procedure cost $7,865.69, however: medicare reimbursement remained the same.Our findings demonstrate a novel use of stenting in the clinic is feasible as an outpatient alternative. It is a safe alternative to the operating room, and more cost-effective.
