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You searched for +publisher:"NSYSU" +contributor:("Steve Leu"). Showing records 1 – 2 of 2 total matches.

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NSYSU

1. Chai, Han-Tan. AG490 Inhibits JAK-2 Activation and Suppresses Anti-Apoptotic Action of Erythropoietin in a Rat Critical Limb Ischemia Model.

Degree: Master, Biological Sciences, 2014, NSYSU

Background: Erythropoietin (EPO) has been demonstrated to enhance recovery in ischemic organ through enhancing angiogenesis. The anti-apoptosis action of EPO was also found in vitro study. To reveal underlying mechanisms and directly examine the benefits of anti-apoptotic capacity of EPO in acute phase of limb ischemia and following blood flow recovery, we applied an experimental critical limb ischemia (CLI) rat model in present study. Methods: To determine the role of JAK2/STATs pathway in EPO-enhanced recovery after CLI, Male Sprague-Dawley rats (n=12 for each group) were divided into group 1 (normal control), group 2 (CLI treated with normal saline), group 3 (CLI treated with EPO), group 4 (CLI treated with AG490, a JAK2 inhibitor), and group 5 (CLI treated with EPO and AG490). Animals were sacrificed at either day 1 or day 14, followed by biochemical and histopathological examination on ischemic quadriceps. Results: At day 1, EPO administration reduced expression levels of apoptotic indices and activated the JAK2/STAT pathway, which inhibited by additional AG490 treatment.Furthermore, the decrease of infarcted area, as well as activation of ERK1/2 and JNK,showed similar regulatory trends with EPO and AG490. Of Interest, EPO and AG490 showed a synergistic effect in increasing expression levels of antioxidants (GR, GPx,NQO-1) and in decreasing transcriptional levels of pro-inflammatory factors (TNF-α,NF-κB). At day 14, laser Doppler analysis showed that the blood flow recovery were enhanced with EPO, AG490, or combined treatment. Conclusion: Although inhibition of JAK2/STAT pathways reduces the anti-apoptotic effects of EPO in early phase of CLI, the benefits of AG490 in anti-inflammation and anti-oxidation still play a positive role in enhancing blood flow recovery after CLI. Advisors/Committee Members: Steve Leu (chair), Chung-Lung Cho (committee member), Chung-Lung Cho (chair), Hsueh-Wen Chang (chair).

Subjects/Keywords: Apoptosis; Critical limb ischemia; JAK2; AG490; Erythropoietin

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

APA (6th Edition):

Chai, H. (2014). AG490 Inhibits JAK-2 Activation and Suppresses Anti-Apoptotic Action of Erythropoietin in a Rat Critical Limb Ischemia Model. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811114-000248

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):

Chai, Han-Tan. “AG490 Inhibits JAK-2 Activation and Suppresses Anti-Apoptotic Action of Erythropoietin in a Rat Critical Limb Ischemia Model.” 2014. Thesis, NSYSU. Accessed April 15, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811114-000248.

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

MLA Handbook (7th Edition):

Chai, Han-Tan. “AG490 Inhibits JAK-2 Activation and Suppresses Anti-Apoptotic Action of Erythropoietin in a Rat Critical Limb Ischemia Model.” 2014. Web. 15 Apr 2021.

Vancouver:

Chai H. AG490 Inhibits JAK-2 Activation and Suppresses Anti-Apoptotic Action of Erythropoietin in a Rat Critical Limb Ischemia Model. [Internet] [Thesis]. NSYSU; 2014. [cited 2021 Apr 15]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811114-000248.

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

Council of Science Editors:

Chai H. AG490 Inhibits JAK-2 Activation and Suppresses Anti-Apoptotic Action of Erythropoietin in a Rat Critical Limb Ischemia Model. [Thesis]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0811114-000248

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


NSYSU

2. Li, Yu-Ru. To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.

Degree: Master, Biological Sciences, 2016, NSYSU

Alzheimer's disease (AD) is one of the common form of age-related neurodegenerative diseases and the leading cause of senile dementia. In the beta-amyloid (Aβ) cascade hypothesis, the aggregation of Aβ is a crucial event that produces amounts of oxidative stress contributed to neurotoxicity. In this study, our hypothesis is that Aβ-peptide aggregation enhances oxidative stress which leads to DNA damage and contributes to neurotoxicity. Therefore, increasing DNA repair efficiency and DNA integrity could rescue neuronal cells from Aβ-induced neuronal death. To test our hypothesis, we utilized lentivirus transduction to overexpress Aβ in rat primary cortical neurons. Results of Western blotting and dihydroethidium (DHE) staining have shown that expression of Aβ reached the peak in the first three days as well as the production of reactive oxygen species (ROS), then both Aβ and ROS levels were decreasing in the following day four to day seven. The DNA damage marker, phosphor-histone 2A (γH2AX), demonstrated that neuronal DNA injury was correlated to both levels of Aβ and ROS. Glucagon-like peptide-1 (GLP-1) is a growth factor which has been proved to have neuroprotective properties. After GLP-1 treatment, the production of Aβ and ROS was reduced, but γH2AX was still remaining in 72 hours. GLP-1 has been proved the effects of decreasing Aβ, inflammation and the improvement of recognition, learning and memory in animal model from previous studies. Although we did not see GLP-1 significantly reducing γH2AX, GLP-1 is still a potential drug involving DNA repair. In Alzheimerâs disease, to elevate DNA repair capability is also a important field to investigate in the future. Advisors/Committee Members: Chen Chun-Lin (committee member), Yang, Jenq-Lin (committee member), Wu, Kay L.H. (chair), Steve Leu (chair).

Subjects/Keywords: β-amyloid; Amyloid precursor protein; Alzheimer's disease; DNA repair; Neurotoxicity

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

APA (6th Edition):

Li, Y. (2016). To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

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):

Li, Yu-Ru. “To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.” 2016. Thesis, NSYSU. Accessed April 15, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537.

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

MLA Handbook (7th Edition):

Li, Yu-Ru. “To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.” 2016. Web. 15 Apr 2021.

Vancouver:

Li Y. To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. [Internet] [Thesis]. NSYSU; 2016. [cited 2021 Apr 15]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537.

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

Council of Science Editors:

Li Y. To Explore β-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. [Thesis]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

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

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