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You searched for +publisher:"NSYSU" +contributor:("Chao, David"). 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 25, 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. 25 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 25]. 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

2. Shi, Jhih-Yin. Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury.

Degree: PhD, Biological Sciences, 2011, NSYSU

Damage to peripheral nerves following trauma or disease has a number of consequences including burning pain, muscle wasting, paralysis, or organ dysfunction. The most common form of neuropathy is that associated with metabolic abnormality, notably diabetes. Many diabetics, especially those with poor blood sugar control, ultimately develop a distal symmetrical and painful neuropathy that initially affects the longest peripheral axons, but with time spreads proximally. Deficiency in neurotrophic support has been proposed to contribute to the development of diabetic neuropathy. Recently, peripheral gene delivery of vascular endothelial growth factor (VEGF), neurotrophin-3 (NT-3), NGF, BDNF or hepatocyte growth factor (HGF) has been shown to facilitate the continuous production of neurotrophic factors and alleviate the diabetic neuropathy. The role of glial cell-derived neurotrophic factor (GDNF) in the pathogenesis and therapeutics of diabetic neuropathy is not well defined. The main objectives of this research sought to inspect the protective effect of GDNF peripheral gene delivery during hyperglycemia- or constriction- induced sciatic nerve injury in rats. In present proposal, we propose to investigate the change in organization and expressions of GDNF signaling complex in the sciatic nerve following injury in the initial stage. Subsequently, the recombinant adenovirus was used gene delivery system for GDNF to evaluate the potential of intramuscular administration of gene delivery for prevent nerve degeneration, and the molecular mechanism of GDNF to ameliorate neuropathy will be clarified. The above study would enable us to test the hypothesis that the topical gene delivery might be a suitable strategy for the treatment of diabetic neuropathy and other disorders in peripheral nerve. Furthermore, the results of animal studies might be extrapolated for future clinical application. Advisors/Committee Members: Huang, Hung-Tu (chair), Chao, David (committee member), Chen, Lee-Wei (chair), Cheng, Jiin-Tsuey (chair), Tai, ming-hong (committee member), Hsu, Ching-Mei (chair).

Subjects/Keywords: Angiogenesis; Diabetes; Diabetic neuropathy; GDNF; Gene delivery

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

APA (6th Edition):

Shi, J. (2011). Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424

Chicago Manual of Style (16th Edition):

Shi, Jhih-Yin. “Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury.” 2011. Doctoral Dissertation, NSYSU. Accessed January 25, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424.

MLA Handbook (7th Edition):

Shi, Jhih-Yin. “Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury.” 2011. Web. 25 Jan 2021.

Vancouver:

Shi J. Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury. [Internet] [Doctoral dissertation]. NSYSU; 2011. [cited 2021 Jan 25]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424.

Council of Science Editors:

Shi J. Glial Cell LineâDerived Neurotrophic Factor Gene Transfer Exerts Protective Effect on Axons in Sciatic Nerve Following Constriction-Induced Peripheral Nerve Injury. [Doctoral Dissertation]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424

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