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Wei-Che Lin,Wen-Chieh Chen,Pei-Wen Wang,Yi-Chia Chan,Yen-Hsiang Chang,Harn-Shen Chen,Szu-Tah Chen,Wei-Chih Chen,Kai-Lun Cheng,Shun-Yu Chi,Pi-Ling Chiang,Chen-Kai Chou,Feng-Fu Chou,Shun-Chen Huang,Feng 대한초음파의학회 2023 ULTRASONOGRAPHY Vol.42 No.3
Radiofrequency ablation (RFA) is a minimally invasive management strategy that has been widely applied for benign and recurrent malignant thyroid lesions as an alternative to surgery in Taiwan. Members of academic societies for specialists in interventional radiology, endocrinology, and endocrine surgery collaborated to develop the first consensus regarding thyroid RFA in Taiwan. The modified Delphi method was used to reach a consensus. Based on a comprehensive review of recent and valuable literature and expert opinions, the recommendations included indications, pre-procedural evaluations, procedural techniques, post-procedural monitoring, efficacy, and safety, providing a comprehensive review of the application of RFA. The consensus effectively consolidates advice regarding thyroid RFA in clinical practice for local experts.
Chun-Yu Liu,Tzu-Ting Huang,Pei-Yi Chu,Chun-Teng Huang,Chia-Han Lee,Wan-Lun Wang,Ka-Yi Lau,Wen-Chun Tsai,Tzu-I Chao,Jung-Chen Su,Ming-Huang Chen,Chung-Wai Shiau,Ling-Ming Tseng,Kuen-Feng Chen 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Triple-negative breast cancer (TNBC) remains difficult to treat and urgently needs new therapeutic options. Nintedanib, a multikinase inhibitor, has exhibited efficacy in early clinical trials for HER2-negative breast cancer. In this study, we examined a new molecular mechanism of nintedanib in TNBC. The results demonstrated that nintedanib enhanced TNBC cell apoptosis, which was accompanied by a reduction of p-STAT3 and its downstream proteins. STAT3 overexpression suppressed nintedanib-mediated apoptosis and further increased the activity of purified SHP-1 protein. Moreover, treatment with either a specific inhibitor of SHP-1 or SHP-1-targeted siRNA reduced the apoptotic effects of nintedanib, which validates the role of SHP-1 in nintedanib-mediated apoptosis. Furthermore, nintedanib-induced apoptosis was attenuated in TNBC cells expressing SHP-1 mutants with constantly open conformations, suggesting that the autoinhibitory mechanism of SHP-1 attenuated the effects of nintedanib. Importantly, nintedanib significantly inhibited tumor growth via the SHP-1/p-STAT3 pathway. Clinically, SHP-1 levels were downregulated, whereas p-STAT3 was upregulated in tumor tissues, and SHP-1 transcripts were associated with improved disease-free survival in TNBC patients. Our findings revealed that nintedanib induces TNBC apoptosis by acting as a SHP-1 agonist, suggesting that targeting STAT3 by enhancing SHP-1 expression could be a viable therapeutic strategy against TNBC.
Chen, Jia,Zheng, Xin,Liu, Dong-Yang,Zhao, Qian,Wu, Yi-Wen,Tan, Fen-Lai,Wang, Yin-Xiang,Jiang, Ji,Hu, Pei Asian Pacific Journal of Cancer Prevention 2014 Asian Pacific journal of cancer prevention Vol.15 No.17
Background: The aim of this study was to evaluate how CYP2C19 affects icotinib and metabolite' exposure, and to determine whether the exposure and EGFR genotype influences survival time, tumor metastasis and adverse drug reactions. Materials and Methods: 274 NSCLC patients who accepted 125mg icotinib/t.i.d. were chosen from a phase III study. Blood samples were obtained in $672^{nd}$ ($4^{th}$ week) and $1,680^{th}$ hours ($10^{th}$ week), and plasma was used to quantify the concentration of icotinib and blood cells were sampled to check the genotypes. Clinical data were also collected at the same time, including EGFR genotypes. Plasma concentrations were assessed by HPLC-MS/MS and genotype by sequencing. All data were analyzed through SPSS 17.0 and SAS 9.2. Results: CYP 2C19 genotypes affected bio-transformation from icotinib to M24 and M26, especially in poor-metabolisers. Higher icotinib concentrations (>1000 ng/mL) not only increased patient PFS and OS but also reduced tumor metastasis. Patients with mutant EGFR experienced a higher median PFS and OS (234 and 627 days), especially those with the 19del genotype demonstrating higher PR ratio. Patients who suffered grade II skin toxicity had a higher icotinib exposure than those with grade I skin toxicity or no adverse effects. Liver toxic reactions might occur in patients with greater M20 and M23 plasma concentrations. Conclusions: CYP2C19 polymorphisms significantly affect icotinib, M24 and M26 exposure. Patients with mutant EGFR genotype and higher icotinib concentration might have increased PFS and OS and lower tumor metastasis. Liver ADR events and serious skin effects might be respectively induced by greater M20, M23 and icotinib concentrations.
Chen Cheng-Hsu,Huang Shih-Chien,Yeh En-Ling,Lin Pei-Chih,Tsai Shang-Feng,Huang Yi-Chia 한국영양학회 2022 Nutrition Research and Practice Vol.16 No.4
BACKGROUND/OBJECTIVES Increased levels of uremic toxins and decreased antioxidant capacity have a significant impact on the progression of chronic kidney disease (CKD). However, it remains unclear whether they interact with each other to mediate the damage of kidney function. The purpose of this study was to investigate whether uremic toxins (i.e., homocysteine and indoxyl sulfate [IS]), as well as glutathione-dependent antioxidant enzyme activities are dependently or independently associated with kidney function during different stages of CKD patients. SUBJECTS/METHODS One hundred thirty-two patients diagnosed with CKD at stages 1 to 5 participated in this cross-sectional study. RESULTS Patients who had reached an advanced CKD stage experienced an increase in plasma uremic toxin levels, along with decreased glutathione peroxidase (GSH-Px) activity. Plasma homocysteine, cysteine, and IS concentrations were all positively associated with each other, but negatively correlated to GSH-Px activity levels after adjusting for potential confounders in all CKD patients. Although plasma homocysteine, cysteine, IS, and GSH-Px levels were significantly associated with kidney function, only plasma IS levels still had a significant association with kidney function after these parameters were simultaneously adjusted. In addition, plasma IS could interact with GSH-Px activity to be associated with kidney function. CONCLUSIONS IS plays a more dominant role than homocysteine and GSH-Px activity in relation to kidney function.
Yi-An Lu,Tuan-Jen Fang,Yu-Cheng Pei,Yun-Chen Tsai,Wan-Ni Lin 대한이비인후과학회 2023 Clinical and Experimental Otorhinolaryngology Vol.16 No.4
Objectives. Laryngeal ultrasonography (LUS) has been suggested as an alternative diagnostic tool for unilateral vocal foldparalysis (UVFP). The present study applied LUS and quantitative laryngeal electromyography (LEMG) in female UVFPpatients to investigate the pathophysiologic mechanisms of UVFP. Methods. In this cross-sectional study, vocal fold (VF) length parameters included resting and phonating VF length measuredusing B-mode LUS, and color Doppler vibrating length (CDVL) measured using the color Doppler mode. Results. Forty female patients with UVFP were enrolled, among whom 11 and 29 were assigned to the thyroarytenoid (TA)muscle+cricothyroid (CT) muscle group (with CT involvement) and the TA (without CT involvement) group, respec-tively. In the TA group, the turn frequency in thyroarytenoid-lateral cricoarytenoid (TA-LCA) on the paralyzed side,as observed through LEMG, correlated with the VF length during the resting phase (R =0.368, P =0.050) and CDVLvalues (R =0.627, P =0.000) on the paralyzed side. In the TA+CT group, the turn ratio in the CT muscle correlatedwith the normalized phonatory vocal length change (nPLC; R =0.621, P =0.041) on the paralyzed side. Conclusion. CDVL and nPLC are two parameters that can be utilized to predict the turn frequencies of TA-LCA in UVFPcases without CT involvement, and the turn ratio of CT in cases of UVFP with CT involvement, respectively. The find-ings suggest that LUS, as a noninvasive tool, can serve as an alternative method for assessing the severity of laryngealnerve injury and offer valuable insights into the pathophysiology of UVFP.