You searched for +publisher:"NSYSU" +contributor:("Tai, ming-hong").
Showing records 1 – 10 of
10 total matches.
No search limiters apply to these results.
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
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0804108-215703 
► 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…
(more)
▼ 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), Hong%22%29&pagesize-30">
Tai,
Ming-
Hong (chair),
Hsu, Ching-Mei (committee member),
Hsu, Li-Chung (chair).
Subjects/Keywords: JNK; Peroxynitrite
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
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 25, 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. 25 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 25].
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
NSYSU
2.
Huang, Chien-Chi.
Pro-oxidant and anti-angiogenic effects of high-dose morphine on the vascular endothelial function and wound healing.
Degree: Master, Biological Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825108-170014
► High-dose morphine has been extensively used in the control of postoperative and cancer pain. Patients receiving prolonged administration of high-dose morphine are known to be…
(more)
▼ High-dose morphine has been extensively used in the control of postoperative and cancer pain. Patients receiving prolonged administration of high-dose morphine are known to be associated with certain cardiovascular complications and tissue regeneration defects. This research thesis aims to investigate the biological effects and molecular mechanisms of high-dose morphine on the vascular endothelial function, angiogenesis and wound regeneration using murine models of morphine-dependence and cultured endothelial cell assays.
Mice were subjected to placebo or morphine (20 mg/kg, i.p.) injection for consecutive 14 days. Aortas were harvested for assessment of vasomotor function by isometric force recordings. Protein expression p47phox (a major subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase) was determined by Western blotting. Generation of superoxide anions was detected under confocal microscope. Endothelium-dependent relaxations to acetylcholine were significantly reduced in morphine-treated animals, but were normalized by superoxide scavenging. Fluorescent densities of dihydroethidium and expression of p47phox were increased in the aorta of morphine-treated mice.
In the second part of this thesis, the candidate determined the effects of high-dose morphine on angiogenesis and mobilization of endothelial progenitor cells (EPCs) in a mouse model of excisional wound injury. Excisional wound was created on control and morphine-dependent mice. Wound healing was compared by measuring the final-to-initial wound area ratio. Generation of superoxide anions in the wound was determined by luminol-enhanced chemiluminescence. Circulating mononuclear cells were isolated and measured for EPC (defined as CD34+/CD133+ cell) counts. In vivo and in vitro measurements of angiogenesis following morphine treatment were performed using the Matrigel assay. The results showed that wound closure was significantly reduced in mice treated with morphine when compared with controls, and higher levels of superoxide anions were generated in these wounds. High-dose morphine reduced numbers of circulating EPCs following creation of excisional wound. Matrigel assay showed impaired angiogenesis in animals and reduced capillary tube formation in cultured endothelial cells treated with high-concentration of morphine.
Collectively, this research thesis demonstrated a number of novel findings. First, high-dose of morphine impairs vascular endothelial function by increased production of vascular superoxide anions. Activation of NADPH oxidase may be the molecular mechanisms responsible for reduced bioavailability of endothelium-derived NO. Second, systemic administration of high-dose morphine delays healing of excisional wounds and impairs angiogenesis. This antiangiogenic effect is associated with increased superoxide anions production and impaired mobilization of EPCs. In line with direct endothelial dysfunction, impaired angiogenesis and EPC mobilization resulted from high-dose morphine treatment may cause increased cardiovascular…
Advisors/Committee Members: Yu-Chuan Tsai (chair), Julie Y.H. Chan (chair), Hong%22%29&pagesize-30">
Tai,
Ming-
Hong (committee member).
Subjects/Keywords: endothelial cell; high-dose morphine; wound healing; angiogenesis
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Huang, C. (2008). Pro-oxidant and anti-angiogenic effects of high-dose morphine on the vascular endothelial function and wound healing. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825108-170014
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):
Huang, Chien-Chi. “Pro-oxidant and anti-angiogenic effects of high-dose morphine on the vascular endothelial function and wound healing.” 2008. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825108-170014.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Huang, Chien-Chi. “Pro-oxidant and anti-angiogenic effects of high-dose morphine on the vascular endothelial function and wound healing.” 2008. Web. 25 Jan 2021.
Vancouver:
Huang C. Pro-oxidant and anti-angiogenic effects of high-dose morphine on the vascular endothelial function and wound healing. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825108-170014.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Huang C. Pro-oxidant and anti-angiogenic effects of high-dose morphine on the vascular endothelial function and wound healing. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825108-170014
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
3.
Chen, Hsuan-yu.
Prognostic Role of Hepatoma-derived growth factor (HDGF) in Breast Cancer.
Degree: Master, Biological Sciences, 2008, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0905108-134315
► Purpose: Hepatoma-derived growth factor (HDGF) is a novel growth factor that plays an important role in the pathogenesis and progression of a variety of cancers.…
(more)
▼ Purpose: Hepatoma-derived growth factor (HDGF) is a novel growth factor that plays an important role in the pathogenesis and progression of a variety of cancers. The present study was designed to elucidate the role of HDGF expression in breast cancer.
Patients and Methods: Tissues were collected from patients with breast cancer who underwent surgery. The expression of HDGF, Ki-67, FOXP3, p53, ER, PR and CD4+CD25+ in 71 patients with breast cancer containing a) malignant tissue (n = 58), b) uninvolved breast tissue obtained from tissue distant from the tumor (n = 13) using immunohistochemistry (IHC). The content of CD4+CD25 high in PBMC was determined by flow cytometry. Data were expressed as ROC Curve and the significance of the differences was assessed by ANOVA.
Results: IHC analysis found that the expression level of HDGF and CD4+CD25high in tumor tissues was significantly higher than that in non-tumor tissues (P < 0.001). Besides, HDGF and CD4+CD25high expression was significantly correlated with tumor grades of breast cancer (P < 0.05). Increased circulating HDGF and CD4+CD25high levels were found in serum from patients with breast cancer compared with serum from healthy controls (P < 0.001). The nuclear HDGF labeling index was positively correlated with Ki-67, FOXP3 and p53 in breast cancer (P < 0.05). Finally, incubation with recombinant HDGF significantly increased the content of CD4(+)CD25high T cells in peripheral blood mononuclear cells (PBMCs).
Conclusion: The present study demonstrated HDGF overexpression is correlated with tumor grades, recurrence, proliferation, and tumor immunity in breast cancer. In the future, HDGF may constitute a novel molecular target for diagnosis and treatment of breast cancer.
Advisors/Committee Members: Hong%22%29&pagesize-30">
Tai Ming-
Hong (committee member),
Hu Tsung-Hui (chair),
Yeh Ming-Hsin (chair).
Subjects/Keywords: HDGF
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, H. (2008). Prognostic Role of Hepatoma-derived growth factor (HDGF) in Breast Cancer. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0905108-134315
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):
Chen, Hsuan-yu. “Prognostic Role of Hepatoma-derived growth factor (HDGF) in Breast Cancer.” 2008. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0905108-134315.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Hsuan-yu. “Prognostic Role of Hepatoma-derived growth factor (HDGF) in Breast Cancer.” 2008. Web. 25 Jan 2021.
Vancouver:
Chen H. Prognostic Role of Hepatoma-derived growth factor (HDGF) in Breast Cancer. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0905108-134315.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen H. Prognostic Role of Hepatoma-derived growth factor (HDGF) in Breast Cancer. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0905108-134315
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
4.
Wu, Ping-Hsuan.
The role of LECT2 in liver carcinogenesis.
Degree: Master, Biological Sciences, 2011, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511
► Leukocyte cell-derived chemotaxin 2 (LECT2) is first isolated as a 16-kDa secreted protein from cultured fluid of phytohemagglutinin-activated human T-cell leukemia SKW-3 cells. Recently LECT2…
(more)
▼ Leukocyte cell-derived chemotaxin 2 (LECT2) is first isolated as a 16-kDa secreted protein from cultured fluid of phytohemagglutinin-activated human T-cell leukemia SKW-3 cells. Recently LECT2 has shown to be synthesized by human hepatocytes and stimulates the growth of chondrocytes. LECT2 is involved in chemotactic factor to neutrophils and may be associated with rheumatoid arthritis. Besides, LECT2 is evolutionarily conserved and acts as a repressor in the Wnt/β-catenin signaling pathway. Wnt/β-catenin signaling is implicated in liver carcinogenesis. However, the exact roles of LECT2 in liver carcinogenesis are not yet well characterized. This study is to investigate the extra roles of LECT2 in Wnt signaling. Our results showed that adenoviral administration of LECT2 over-expression suppress oncogenic processes such as migration, invasion, proliferation and colony formation, as well as alteration in cell cycle distributions. In animal model significantly suppress liver malignancies in orthotopic Novikoff hepatoma. In conclusion, we show that ad-LECT2 gene delivery attenuated cell carcinogenesis process via downregulated Wnt/β-catenin signaling in vitro and suppressed tumor growth in vivo. Besides LECT2 over-expression represents a novel therapeutically factor for hepatocelluar carcinoma.
Advisors/Committee Members: Cheng, Jiin-Tsuey (chair), Hu, Tsung-Hui (chair), Hong%22%29&pagesize-30">
Tai,
Ming-
Hong (committee member).
Subjects/Keywords: Wnt pathway; β-catenin; Hepatocellular carcinoma; cellular signaling; LECT2
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wu, P. (2011). The role of LECT2 in liver carcinogenesis. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511
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):
Wu, Ping-Hsuan. “The role of LECT2 in liver carcinogenesis.” 2011. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Ping-Hsuan. “The role of LECT2 in liver carcinogenesis.” 2011. Web. 25 Jan 2021.
Vancouver:
Wu P. The role of LECT2 in liver carcinogenesis. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu P. The role of LECT2 in liver carcinogenesis. [Thesis]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0824111-001511
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
5.
Chen, Chueh-Tan.
The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure.
Degree: Master, Biological Sciences, 2012, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0216112-112117
► Lead (Pb) is one of the most well known toxic heavy metals in human beings and animals, which leads to toxic neurological disorders, cognitive problems,…
(more)
▼ Lead (Pb) is one of the most well known toxic heavy metals in human beings and animals, which leads to toxic neurological disorders, cognitive problems, learning and memory disabilities. Epidemiological studies revealed that chronic lead exposure is one of the environmental risk factors which may cause Alzheimerâs Disease, which were speculated for the observation of cellular necrosis, apoptosis, and β-amyloid deposition frequently occuring altogether after chronic lead exposure. Recent studies have shown that the β-amyloid formed during autophagic turnover of APP-rich organelles supplied by both autophagy and endocytosis. Therefore, we will conduct the new perspective for studying the possible role of autophagy on amyloidogensis disorders after lead exposure. SH-SY5Y human neuroblastoma cells, used in this study, were differentiated to a neuronal phenotype by retinoic acid (RA) to the culture medium at 10 μM for 1, 2, 3 and 4 days. Doses of lead acetate with of lead acetate were 5 μM and applied to the neuronal culture and then cell viability measurement by MTT assay. The apoptotic effect of non-differentiation and differentiation neuroblastoma cells after lead exposure was determined by cleaved DNA fragments. Furthermore, APP, intracellular Aβ1-40 and Aβ1-42 expression were quantified by Real-time PCR and ELISA, respectively. The autophagy process and variation of total and phosphorylated mammalian target of rapamycin (mTOR) forms were determined after lead exposure in non-differentiation and differentiation neuroblastoma cells by western blot. The results indicate that lead exposure enhances autophagy response in both non-differentiation and differentiation SH-SY5Y cells, which might cause neuronal apoptosis associated with β-amyloidgenesis. Otherwise, lead exposure resulted in the inhibition of mTOR signaling, which correlated with the autophagic process. Besides, in our studies, non-differentiated cells exhibited more toxic vulnerability than RA induced differentiated neuron is congruous to previous finding that lead exposure during fetal development might be a potential risk factor for AD in the adulthood.
Advisors/Committee Members: Chen,Tsan-Ju (chair), Cheng, Jiin-Tsuey (committee member), Hong%22%29&pagesize-30">
Tai,
Ming-
Hong (chair),
Chen, Shun-Sheng (committee member).
Subjects/Keywords: Alzheimerâs Disease; amyloid precursor protein; autophagy; amyloidogensis disorders; apoptosis; β-amyloid protein; lead exposure
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chen, C. (2012). The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0216112-112117
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):
Chen, Chueh-Tan. “The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure.” 2012. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0216112-112117.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Chueh-Tan. “The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure.” 2012. Web. 25 Jan 2021.
Vancouver:
Chen C. The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0216112-112117.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen C. The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure. [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0216112-112117
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
6.
Shen, Ying-Ying.
Generation and Characterization of Recombinant Adenovirus Encoding Irisin.
Degree: Master, Institute of Biomedical Sciences, 2017, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0722117-235342
► Exercise represents one of the most effective approaches for control of obesity and metabolic syndromes. Irisin is a 112-residue myokine secreted by skeletal muscle through…
(more)
▼ Exercise represents one of the most effective approaches for control of obesity and metabolic syndromes. Irisin is a 112-residue myokine secreted by skeletal muscle through proteolytical cleavage from its precursor fibronectin type III domain containing 5 (FNDC5). Irisin stimulates brown fat-like development from white fat and thermogenesis through increasing mitochondria genesis and energy expenditure, thereby reducing body weight and insulin resistance. Because of its anti-obesity effects and evolutionary conservation, Irisin has been proposed as a promising therapeutic agent for metabolic diseases since its discovery in 2012. To combat the obesity syndrome, gene therapy approached may be required for long-term management of patients with metabolic diseases. Thus, the present study aims to generate the recombinant adenovirus vectors for Irisin production in various types of cells/organs, thereby evaluating their therapeutic potential and mechanism. Recombinant irisin was expressed and purified from E. coli with an apparent molecular weight of 14 kDa. The anti-irisin antibody was raised by periodical injection of recombinant irisin into rabbit and purified from serum using protein G Sepharose affinity chromatography. For gene delivery, adenovirus vector encoding FNDC5 (Ad-FNDC5) and irisin (Ad-irisin) were generated and purified by cesium chloride ultracentrifugation. To investigate the profile of FNDC5/irisin expression in different types of cells, endothelial EA.hy926, muscle C2C12, hepatocytes Clone-9, and embryonic kidney HEK293 cells were employed for adenovirus gene delivery. By immunoblot analysis and enzyme-linked immunoassay (ELISA), it was found that Ad-irisin effectively transduced and conferred irisin secretion in all four types of cells whereas Ad-FNDC5 evoked moderate irisin secretion only in C2C12 and Clone-9 cells. Infection with Ad-irisin enhanced the viability and migration of endothelial cells, supporting the pro-angiogenic function of irisin. Besides, Ad-irisin-infected hepatocytes exhibited elevated activities of AMPK/Akt and inhibition of PEPCK signaling, suggesting the role of irisin in gluconeogenesis in the livers. With the development of these irisin-based tools, future studies are warranted to elucidate the cellular function of irisin in different organs, thereby exploring the therapeutic potential of irisin therapy for various human diseases.
Advisors/Committee Members: Sheu, Jim Jinn-Chyuan (chair), Chen, Chun-Lin (chair), Hong%22%29&pagesize-30">
Tai,
Ming-
Hong (committee member).
Subjects/Keywords: angiogenesis; gene therapy; obesity; myokines; Irisin; gluconeogenesis
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Shen, Y. (2017). Generation and Characterization of Recombinant Adenovirus Encoding Irisin. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0722117-235342
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):
Shen, Ying-Ying. “Generation and Characterization of Recombinant Adenovirus Encoding Irisin.” 2017. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0722117-235342.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Shen, Ying-Ying. “Generation and Characterization of Recombinant Adenovirus Encoding Irisin.” 2017. Web. 25 Jan 2021.
Vancouver:
Shen Y. Generation and Characterization of Recombinant Adenovirus Encoding Irisin. [Internet] [Thesis]. NSYSU; 2017. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0722117-235342.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Shen Y. Generation and Characterization of Recombinant Adenovirus Encoding Irisin. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0722117-235342
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
7.
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
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424
► 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…
(more)
▼ 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), hong%22%29&pagesize-30">
Tai,
ming-
hong (committee member),
Hsu, Ching-Mei (chair).
Subjects/Keywords: Angiogenesis; Diabetes; Diabetic neuropathy; GDNF; Gene delivery
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
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
NSYSU
8.
Chung, Yueh-hua.
The role and effect of bone morphogenetic protein-2 in liver fibrosis.
Degree: Master, Biological Sciences, 2007, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0827107-112806
► Bone Morphogenetic proteins (BMPs) belong to transforming growth factor beta (TGF-β) superfamily. They regulate cell proliferation, cell differentiation, and bone morphogenesis. Previous evidence suggests that…
(more)
▼ Bone Morphogenetic proteins (BMPs) belong to transforming growth factor beta (TGF-β) superfamily. They regulate cell proliferation, cell differentiation, and bone morphogenesis. Previous evidence suggests that BMP-2, as an antagonist of TGF-β, may play an inhibitory role in tissue fibrogenesis. The aim of this study is to examine the expression profile of BMP-2 in fibrotic livers and to test whether BMP-2 gene delivery could alleviate or reverse the liver fibrogenesis models in mice including bile duct ligation (BDL) or carbon tetrachloride (CCl4) model. The results showed that the AST, ALT, and bilirubin levels in sera and the expression of TGF-β, α-smooth muscle actin, type I collagen in livers were significantly up-regulated by BDL surgery or CCl4 administration. After BDL, the hepatic BMP-2 mRNA and protein levels in mice decreased at 7 and 14 days after surgery. Similarly, the hepatic BMP-2 mRNA and protein levels in mice decreased at day 14 and 28 after CCl4 administration. BMP-2 gene delivery alleviated the inflammation and the liver injury caused by BDL or CCl4 exposure. These findings strongly suggest that BMP-2 is involved in the pathogenesis of liver fibrosis. Moreover, BMP-2 supplementation may facilitate a novel strategy for treatment of liver fibrosis.
Advisors/Committee Members: Cho Chung-Lung (chair), Hong%22%29&pagesize-30">
Tai Ming-
Hong (committee member),
Hu Tsung-hui (chair).
Subjects/Keywords: liver fibrosis; Bone morphogenetic protein-2
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chung, Y. (2007). The role and effect of bone morphogenetic protein-2 in liver fibrosis. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0827107-112806
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):
Chung, Yueh-hua. “The role and effect of bone morphogenetic protein-2 in liver fibrosis.” 2007. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0827107-112806.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chung, Yueh-hua. “The role and effect of bone morphogenetic protein-2 in liver fibrosis.” 2007. Web. 25 Jan 2021.
Vancouver:
Chung Y. The role and effect of bone morphogenetic protein-2 in liver fibrosis. [Internet] [Thesis]. NSYSU; 2007. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0827107-112806.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chung Y. The role and effect of bone morphogenetic protein-2 in liver fibrosis. [Thesis]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0827107-112806
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
9.
Huang, Wen-hung.
Effect and mechanism of 6-OHDA induced inflammation in rat urinary bladder and prostate.
Degree: Master, Biological Sciences, 2007, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626107-112159
► The mechanisms underlying the 6-hydroxydopamine (6-OHDA)-induced inflammatory response in the urinary bladder and prostate in anaesthetized male rats of Long- Evan strain were investigated. The…
(more)
▼ The mechanisms underlying the 6-hydroxydopamine (6-OHDA)-induced inflammatory response in the urinary bladder and prostate in anaesthetized male rats of Long- Evan strain were investigated. The magnitude of inflammatory responses were evaluated by morphometric analysis of the area density of India ink-labeled blood vessels in urinary bladder whole mounts and spectrophotometric analysis of Evans blue dye contents in urinary bladder and prostate. Moreover, scanning electron microscopy was employed to observe the venular endothelium in the urinary bladder wall and glandular epithelium in the prostate gland. Fifteen minutes after local application of 6-OHDA to the urinary bladder, 6-OHDA induced an increase of plasma leakage in a dose-dependent manner. It was revealed that area densities of India ink-labeled blood vessels in the rat urinary bladder whole mount were 5.65±1.72 % (N=6), 22.63±3.12 % (N=6), and 35.02±2.25 % (N=6) respectively, following a local injection of vehicle, 5 mg/kg 6-OHDA, and 10 mg/kg 6-OHDA. Using Evans blue dye as a tracer for spectrophotometric analysis, the results were similar. The Evans blue dye content was 80.53±60.74 ng/mg in the urinary bladder and 48.81±2.83 ng/mg in the prostate following injection of 5 mg/kg 6-OHDA (N=6). The Evans blue dye content was 157.73±4.45 ng/mg in the bladder and 65.52±4.25 ng/mg in the prostate following injection of 10 mg/kg 6-OHDA (N=6). Evans blue dye contents in the vehicle group (N=6) were much lower, 18.82±3.74 ng/mg in the urinary bladder and 18.50±2.47 ng/mg in the prostate, which were significantly smaller than the 6-OHDA treated group. Interestingly, the inflammatory responses were completely abolished by pretreating alone with dimethylthiourea (DMTU), a hydroxyl radical scavenger, and were moderately attenuated by pretreatment with L-732,138, a NK1 receptor antagonist. Under scanning electron microscope observation, 6-OHDA caused endothelial gaps formation in the venules of urinary bladder wall and triggered the release of secretory granules in the prostate gland cells. We concluded that 6-OHDA could induce inflammation in the urinary bladder and prostate gland involving free radical and tachykinin mechanisms.
Advisors/Committee Members: Shiping He (chair), Huang, Hung-Tu (committee member), Hong%22%29&pagesize-30">
Tai,
Ming-
Hong (chair).
Subjects/Keywords: plasma leakage; 6-OHDA; inflammatory response; prostate; urinary bladder
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Huang, W. (2007). Effect and mechanism of 6-OHDA induced inflammation in rat urinary bladder and prostate. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626107-112159
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):
Huang, Wen-hung. “Effect and mechanism of 6-OHDA induced inflammation in rat urinary bladder and prostate.” 2007. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626107-112159.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Huang, Wen-hung. “Effect and mechanism of 6-OHDA induced inflammation in rat urinary bladder and prostate.” 2007. Web. 25 Jan 2021.
Vancouver:
Huang W. Effect and mechanism of 6-OHDA induced inflammation in rat urinary bladder and prostate. [Internet] [Thesis]. NSYSU; 2007. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626107-112159.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Huang W. Effect and mechanism of 6-OHDA induced inflammation in rat urinary bladder and prostate. [Thesis]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0626107-112159
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
10.
Wu, Chia-Ling.
The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.
Degree: Master, Biological Sciences, 2004, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607
► Dlk is a transmembrane protein that possesses six epidermal growth factor-like sequences at the extracellular domain, a single transmembrane domain and an intracellular tail. The…
(more)
▼ Dlk is a transmembrane protein that possesses six epidermal growth factor-like sequences at the extracellular domain, a single transmembrane domain and an intracellular tail. The extracellular EFG-like region of Dlk can be released by action of an unknown protease that cuts the extracellular region near the cell membrane. Dlk belongs to the EGF-like homeotic protein family and has received many names: pG2, FA-1, Pref-1, SCP-1, ZOG and Dlk. All the proteins are identical or polymorphic products of a single gene. Dlk has been involved in several differentiation processes, such as adipogenesis, hematopoiesis and neuroendocrine differentiation. Dlk is also known as the preadipocyte factor-1 (Pref-1), is highly expressed in preadipocytes but is completely abolished in adipocytes. Pref-1 may function in the maintenance of the preadipocyte state and is a negative regulator of adipocyte differentiation.
Dlk is expressed in tumors with neuroendocrine features, such as human neuroblastoma, rat pheochromocytoma, and a subset of Small Cell Lung Cancer (SCLC) cell lines. The Dlk expression is probably associated with some differentiation stages because the most undifferentiated cells were lacking expression of Dlk. The finding suggests that Dlk plays an important role in differentiation and tumorigenesis of several cell types.
The study was designed to examine the influence of dlk overexpression on tumorigenicity of hepatoma cells. We constructed the mammalian expression vectors for full-length dlk, dlk extracellular domain, which were transfected into SK-Hep-1 cells for generation of stable clones. The transgene expressions in selected stable clones were verified by QRT-PCR and western blot analysis. Our results indicated that overexpression of extracellular domain significantly promoted the viability of SK-Hep1 cells during serum deprivation. In SCID mice, injection of full-length dlk clones led to increased tumor growth compared with the control groups. However, the migration ability was reduced in Dlk stable clones. In summary, these results suggested full-length Dlk promoted the tumor growth but reduced the migration ability of SK-Hep1 cells.
Advisors/Committee Members: Cho Chung-Lung (chair), Hong%22%29&pagesize-30">
Tai Ming-
Hong (committee member),
Cheng Jiin-Tsuey (chair),
Chuang Jiin-Haur (committee member).
Subjects/Keywords: overexpression; tumorigenicity; hepatoma cells; Dlk protein
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Wu, C. (2004). The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607
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):
Wu, Chia-Ling. “The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.” 2004. Thesis, NSYSU. Accessed January 25, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Wu, Chia-Ling. “The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.” 2004. Web. 25 Jan 2021.
Vancouver:
Wu C. The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. [Internet] [Thesis]. NSYSU; 2004. [cited 2021 Jan 25].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Wu C. The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. [Thesis]. NSYSU; 2004. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904104-203607
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
. 
Open Access Theses and Dissertations
