Open Library Archives of Kagawa University (OLIVE)
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Correlation of epidermal growth factor receptor mutation status and PD-L1 expression with [18F]FDG PET using volume-based parameters in non-small cell lung cancer
Get PDF香川大学Kagawa University博士（医学）Objective: We investigated the relationship between 2-deoxy-2-[18F]fluoro-D-glucose (FDG) PET using volume-based parameters and epidermal growth factor receptor (EGFR) mutation status, programmed death-ligand-1 (PD-L1) expression level, and their combination, in pretreated non-small cell lung cancer (NSCLC).Methods: FDG PET findings and EGFR mutation status and PD-L1 expression level were investigated retrospectively in 93 patients with newly diagnosed NSCLC (77 adenocarcinomas, 16 squamous cell carcinomas). Tumors were divided into six groups: EGFR mutant/negative PD-L1, EGFR mutant/low PD-L1, EGFR mutant/high PD-L1, EGFR wild/negative PD-L1, EGFR wild/low PD-L1, and EGFR wild/high PD-L1. The maximum standardized uptake value (SUVmax), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) for primary tumor were measured from PET images. The EGFR mutation status and PD-L1 expression level were estimated in tumor tissue specimens and compared with the PET parameters.Results: None of the PET parameters differed significantly between EGFR-mutated and wild-type EGFR. According to the PD-L1 level, significant differences were detected in SUVmax (P = 0.001) and TLG (P = 0.016), but not MTV. Comparing all six groups, significant difference was detected in only SUVmax (P = 0.011).Conclusion: Based on the preliminary results of this study, FDG PET may help in the prediction of PD-L1 expression level, but not EGFR mutation status, in patients with newly diagnosed NSCLC. The SUVmax rather than MTV or TLG, may be of value in predicting the six groups according to the combination of EGFR mutation status and PD-L1 expression level.doctoral thesi
Development of a Myoelectric Pattern-Based User Interface for Home Appliance Control for Individuals with Disabilities
Get PDF現代の様々なユーザインタフェースは、我々の生活利便性を大きく向上させてきた。その一方で、身体的制約を持つ人々、特に重度重複障害を持った人にとって、従来のマウス、キーボード、リモコンのスイッチ等は、手指の細かい操作を必要とする場合が多く、十分にアクセシブルなものとは言えなかった。そこで本研究では、意識的な大きな動作を必要としない「微小筋電信号」を活用することで、重度重複障害を持った人でも利用可能な家電制御用ユーザインタフェース・システムを提案する。微小筋電信号は、極めて微弱な筋肉の動きに伴い発生し、この電気信号をユーザインタフェースのトリガーとして家電の制御を行う。このため、特に運動能力が著しく制限された障害を持った人に特に有用であると考える。このインタフェースが実現できれば、重度重複障害を持った人自らが、様々な機器の制御が行えるだけでなく、他者とのコミュニケーションの可能性を生みだし、ひいては、能動的な態度から自らが持つ自律的な生き方を実現する事も期待できる。departmental bulletin pape
Therapeutic Effect of Proteinase-Activated Receptor-1 Antagonist on Colitis-Associated Carcinogenesis
Get PDF香川大学Kagawa University博士（医学）Background & aims: Inflammatory bowel disease is associated with carcinogenesis, which limits the prognosis of the patients. The local expression of proteinases and proteinase-activated receptor 1 (PAR1) increases in inflammatory bowel disease. The present study investigated the therapeutic effects of PAR1 antagonism on colitis-associated carcinogenesis.Methods: A colitis-associated carcinogenesis model was prepared in mice by treatment with azoxymethane (AOM) and dextran sulfate sodium (DSS). PAR1 antagonist E5555 was administered in long- and short-term protocol, starting on the day of AOM injection and 1 week after completing AOM/DSS treatment, respectively. The fecal samples were collected for metagenome analysis of gut microbiota. The intestinal myofibroblasts of the Crohn's disease patients were used to elucidate underlying cellular mechanisms. Caco-2 cells were used to investigate a possible source of PAR1 agonist proteinases.Results: AOM/DSS model showed weight loss, diarrhea, tumor development, inflammation, fibrosis, and increased production of inflammatory cytokines. The β-diversity, but not α-diversity, of microbiota significantly differed between AOM/DSS and control mice. E5555 alleviated these pathological changes and altered the microbiota β-diversity in AOM/DSS mice. The thrombin expression was up-regulated in tumor and non-tumor areas, whereas PAR1 mRNA expression was higher in tumor areas compared with non-tumor areas. E5555 inhibited thrombin-triggered elevation of cytosolic Ca2+ concentration and ERK1/2 phosphorylation, as well as IL6-induced signal transducer and activator of transcription 3 (STAT3) phosphorylation in intestinal myofibroblasts. Caco-2 cell-conditioned medium contained immunoreactive thrombin, which cleaved the recombinant protein containing the extracellular domain of PAR1 at the thrombin cleavage site.Conclusions: PAR1 antagonism is proposed to be a novel therapeutic strategy for treatment of inflammatory bowel disease and its associated carcinogenesis.doctoral thesi
