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You searched for +publisher:"NSYSU" +contributor:("Lin, Meng-Chih"). Showing records 1 – 2 of 2 total matches.

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NSYSU

1. Wang, Ting-ya. Suppression of High Mobility Group Box-1 (HMGB-1) by RNAi Might Alter the Inflammatory Response During Sepsis.

Degree: Master, Biological Sciences, 2008, NSYSU

High mobility group box 1 (HMGB-1) protein is a non-histone chromosomal protein. As a DNA binding protein, HMGB-1 is involved in the maintenance of nucleosome structure, regulation of gene transcription and it is active in DNA recombination and repair. It has been known that HMGB-1 is a late mediator of endotoxemia and sepsis. HMGB-1 is released from activated macrophages, induces the release of other proinflammatory mediators, and mediates cell death when overexpressed. We speculated that the course of sepsis maybe different without the involvement of HMGB-1. The aims of this study are to investigate the role of HMGB-1 in mediating sepsis and to observe the effects by using RNAi to affect the production of HMGB-1. Lipopolysaccharide (LPS) was used to simulate sepsis in culture as well as stimulate the release of HMGB-1 from RAW 264.7 cells. Levels of HMGB-1 in the culture medium were subsequently measured by Western blot. Other proinflammatory cytokines (TNF-α, IL-6 and TGF-β) were measured by ELISA. HMGB-1 could not be detected in the culture medium in the absence of LPS stimuli, but after 0.5 μg/ml LPS treatment HMGB-1 release could be detected. HMGB-1 the amount of released from LPS activated RAW 264.7 cells was in a time- and dose-dependent manner. The present study demonstrated that RNAi in the treatment of LPS-stimulated RAW264.7 cells resulted in the blockade of HMGB-1 and decreased LPS-induced inflammatory response. The results demonstrated that HMGB-1 plays a pivotal role in macrophage inflammatory responses by modulating the production of inflammatory mediators. Advisors/Committee Members: Cho, Chung-Lung (chair), Chao, David (committee member), Lin, Meng-Chih (chair).

Subjects/Keywords: RNA interference (RNAi); sepsis; cytokine; High mobility group box 1 (HMGB1)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Wang, T. (2008). Suppression of High Mobility Group Box-1 (HMGB-1) by RNAi Might Alter the Inflammatory Response During Sepsis. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904108-164845

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Wang, Ting-ya. “Suppression of High Mobility Group Box-1 (HMGB-1) by RNAi Might Alter the Inflammatory Response During Sepsis.” 2008. Thesis, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904108-164845.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Wang, Ting-ya. “Suppression of High Mobility Group Box-1 (HMGB-1) by RNAi Might Alter the Inflammatory Response During Sepsis.” 2008. Web. 18 Jan 2021.

Vancouver:

Wang T. Suppression of High Mobility Group Box-1 (HMGB-1) by RNAi Might Alter the Inflammatory Response During Sepsis. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904108-164845.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Wang T. Suppression of High Mobility Group Box-1 (HMGB-1) by RNAi Might Alter the Inflammatory Response During Sepsis. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904108-164845

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


NSYSU

2. Kuo, Fu-chen. Detection of EGFR Mutation by Cell-Free DNA in Pleural Effusion of Lung Adenocarcinoma.

Degree: Master, Biological Sciences, 2015, NSYSU

Epidermal growth factor receptor (EGFR) mutation status is important for the selection of the candidates for target therapy with tyrosine kinase inhibitor in lung adenocarcinomas. However, the specimens for analysis of EGFR mutation are usually derived from invasive procedures and not always available. To increase the availability and sensitivity of EGFR mutation detection, we used a highly sensitive Taqman Mutation Detection Assay (TMDA) for EGFR mutation analysis in 70 patients of malignant pleural effusion, including 50 patients previously analyzed for EGFR mutation by Sanger sequencing or real-time PCR method on either biopsy/surgical specimen or cell block of pleural effusion. Cell-free DNA in pleural effusion was isolated to perform EGFR analysis by this assay. A comparison of the EGFR mutation status between the cell-free DNA of pleural effusion and the previous specimen from the same patient was also made. EGFR mutations mainly occur in the tyrosine kinase domain, exons 18â21, in which deletions in exon 19 and point mutation in exon 21 (L858R) account for approximately 90%, therefore the main EGFR mutation testing in the present study has focused on exon 19 deletions and L858R mutation. The result showed no signal in 3 out of the 70 patients, which may be due to insufficient amount of DNA. In the other 67 patients, 40 (59.7%) of them showed L858R mutation or exon 19 deletions. There are 26 patients (65%) with L858R mutation and 20 patients (50%) with exon 19 deletions. Both L858R mutation and exon 19 deletions are found in 6 patients, accounting for 15% in all EGFR mutation cases. Our study indicates that TMDA is a feasible technique to detect EGFR mutation status in malignant pleural effusion, and potentially useful for the discovery of false-negative cases analyzed by Sanger sequencing. The malignant pleural effusion could be firstly used for EGFR mutation analysis to shorten the turnaround time. Advisors/Committee Members: Lin, Meng-Chih (chair), Chun-lin Chen (chair), Chao-Cheng Huang (committee member), Jiin-Tsuey Cheng (committee member).

Subjects/Keywords: Lung adenocarcinoma; EGFR mutation; malignant pleural effusion; Taqman Mutation Detection Assay; cell-free DNA; real-time PCR

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

Kuo, F. (2015). Detection of EGFR Mutation by Cell-Free DNA in Pleural Effusion of Lung Adenocarcinoma. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0026115-222600

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

Kuo, Fu-chen. “Detection of EGFR Mutation by Cell-Free DNA in Pleural Effusion of Lung Adenocarcinoma.” 2015. Thesis, NSYSU. Accessed January 18, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0026115-222600.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

Kuo, Fu-chen. “Detection of EGFR Mutation by Cell-Free DNA in Pleural Effusion of Lung Adenocarcinoma.” 2015. Web. 18 Jan 2021.

Vancouver:

Kuo F. Detection of EGFR Mutation by Cell-Free DNA in Pleural Effusion of Lung Adenocarcinoma. [Internet] [Thesis]. NSYSU; 2015. [cited 2021 Jan 18]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0026115-222600.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kuo F. Detection of EGFR Mutation by Cell-Free DNA in Pleural Effusion of Lung Adenocarcinoma. [Thesis]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0026115-222600

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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