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You searched for +publisher:"NSYSU" +contributor:("Chen, Lee-Wei"). Showing records 1 – 2 of 2 total matches.

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NSYSU

1. Tseng, Hsiu- Ting. Peritonitis-induced Peroxynitrite Production of Hematopoietic Cells and Lung Damage Depends on the JNK Signaling Pathway.

Degree: Master, Biological Sciences, 2008, NSYSU

Abdominal sepsis is a common, life-threatening condition in the critically ill patients. The c-Jun N-terminal kinase (JNK) is known as a stress-activated protein kinase, in order to study the role of JNK on peritonitis-induced lung injury, the changes of plasma dihydrorhodamine 123 (DHR 123) oxidation level; the myeloperoxidase (MPO) and extravasations of Evans blue dye (EBD) of lung in wild-type (WT) mice with P. aeruginosa-induced peritonitis were determined first. Second, the specific JNK inhibitor, SP600125 or lefunomide, was given to WT mice immediately after P. aeruginosa injection and DHR oxidation, MPO activity, and EBD extravasations were examined. Third, JNK1-/- mice and JNK1+/- mice were subjected to peritonitis and assayed for DHR 123 oxidation, MPO activity, EBD extravasations, and reactive oxygen species (ROS). Fourth, chimeric mice (WT â WT, JNK1-/- â WT, WTâJNK1-/-) were generated and used to determine the role of hematopoietic cells in peritonitis-induced lung damage. The results show that peritonitis induced DHR 123 oxidation; MPO activity and EBD extravasations in lungs and administration of specific JNK inhibitor decreased the peritonitis-induced DHR oxidation and lung damage. Also, both JNK1-/- and JNK1+/- mice showed a decreased DHR oxidation and lung damage after peritonitis. Finally, the decrease of DHR 123 oxidation, ROS, and lung damage in JNK1-/- â WT chimeric mice suggests that that peritonitis-induced expression of iNOS and subsequent peroxynitrite production and lung damage depends on the JNK1 signaling of the hematopoietic cells. Advisors/Committee Members: Chen, Lee-Wei (committee member), Tai, Ming-Hong (chair), Hsu, Ching-Mei (committee member), Hsu, Li-Chung (chair).

Subjects/Keywords: JNK; Peroxynitrite

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

APA (6th Edition):

Tseng, H. T. (2008). Peritonitis-induced Peroxynitrite Production of Hematopoietic Cells and Lung Damage Depends on the JNK Signaling Pathway. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804108-215703

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):

Tseng, Hsiu- Ting. “Peritonitis-induced Peroxynitrite Production of Hematopoietic Cells and Lung Damage Depends on the JNK Signaling Pathway.” 2008. Thesis, NSYSU. Accessed January 17, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804108-215703.

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

MLA Handbook (7th Edition):

Tseng, Hsiu- Ting. “Peritonitis-induced Peroxynitrite Production of Hematopoietic Cells and Lung Damage Depends on the JNK Signaling Pathway.” 2008. Web. 17 Jan 2021.

Vancouver:

Tseng HT. Peritonitis-induced Peroxynitrite Production of Hematopoietic Cells and Lung Damage Depends on the JNK Signaling Pathway. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 17]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804108-215703.

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

Council of Science Editors:

Tseng HT. Peritonitis-induced Peroxynitrite Production of Hematopoietic Cells and Lung Damage Depends on the JNK Signaling Pathway. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804108-215703

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 17, 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. 17 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 17]. 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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