+publisher:"NSYSU" +contributor:("Cheng Jiin-Tsuey")

NSYSU

1. Kuo, Yu-Fen. POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells.

Degree: Master, Biological Sciences, 2008, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731

► Melanoma is a cancer of the pigment producing cells, melanocytes, and is the most serious type of skin cancer. Cancer is a condition in which… (more)

▼ Melanoma is a cancer of the pigment producing cells, melanocytes, and is the most serious type of skin cancer. Cancer is a condition in which one type of cell grows without limit in a disorganized fashion, disrupting and replacing normal tissues and their functions. Normal melanocytes reside in the outer layer of the skin and produce a brown pigment called melanin, which is responsible for skin color. Melanoma occurs when melanocytes become cancerous, grow, and invade other tissues. Pro-opiomelanocortin (POMC) is a precursor polypeptide of 241 amino acids and the prohormone of various neuropeptide, including corticotropin (ACTH), Î±-melanocyte-stimulating hormone (Î±-MSH), and Î²-endorphin (Î²-EP). Recently, we demonstrated that systemic POMC overexpression potently suppresses the growth and metastasis of B16-F10 melanoma in vitro and in vivo. However, despite potent inhibition of tumor proliferation and angiogenesis, B16-F10 melanoma still managed to survive after POMC gene therapy. The underlying survival mechanism of B16-F10 melanoma remains unclear. Microphthalmia-associated transcription factor (MITF) is a basic helix-loop-helix transcription factor that plays a key role not only in melanin synthesis, but also in melanocyte development and survival. Besides, MITF binds to the hypoxia-inducible factor-1Î± (HIF-1Î±) promoter to stimulate its transcriptional activity. In this study, we investigate the influence of POMC gene delivery on the pro-survival MITF/HIF-1Î± pathway in B16-F10 melanoma cells. Quantitative RT-PCR and western blot analysis revealed that POMC gene delivery increased the MITF mRNA and protein level in B16-F10 melanoma cells. Besides, POMC gene delivery significantly enhanced the HIF-1Î±-driven luciferase activities in melanoma cells. By transfection and puromycin selection, we generated and characterized a MITF-knockdown B16-F10 melanoma cells (MITF KD) stably expressing short hairpin RNA against MITF. The growth, invasion, and colonies formation of MITF-KD were similar to those of vector control. However, implantation of MITF-KD cells led to melanoma with significantly reduced tumor size compared with those in mice implanted with vector control cells. Histological analysis revealed a significant reduction of CD31-positive blood vessels in implantation of MITF-KD cells-treated tumors, which was accompanied with a decrease in Ki-67-positive proliferating cells and an increase in TUNEL-positive apoptotic cells. Moreover, POMC-mediated upregulation of MITF and HIF-1 Î± was significantly attenuated in MITF KD-B16-F10 cells. Acetylsalicylic acid (aspirin; ASA) is widely used as an analgesic/antipyretic drug. ASA exhibits a wide range of biological effects, including preventative effects against heart attack, stroke, and the development of some types of cancer. In our study, we found ASA enhanced cell proliferation. However, in invasion test, ASA had no effect on cell migration. POMC gene delivery elevated the mRNA and protein level of hemeoxygenase-1 (HO-1), a downstream effector of HIF-1Î± pathway… Advisors/Committee Members: Ming-Hong Tai (committee member), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (chair), HONG YI-REN (chair).

Subjects/Keywords: Heme oxygenase-1; Adenovirus; Proopiomelanocortin; melanoma

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Kuo, Y. (2008). POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731

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

Chicago Manual of Style (16^th Edition):

Kuo, Yu-Fen. “POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells.” 2008. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731.

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

MLA Handbook (7^th Edition):

Kuo, Yu-Fen. “POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells.” 2008. Web. 07 Mar 2021.

Vancouver:

Kuo Y. POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells. [Internet] [Thesis]. NSYSU; 2008. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731.

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

Council of Science Editors:

Kuo Y. POMC Overexpression Stimulates MITF/HIF-1Î± Survival Pathway in B16-F10 Melanoma Cells. [Thesis]. NSYSU; 2008. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0901108-100731

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

NSYSU

2. Wang, Yin-Hsuan. The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells.

Degree: Master, Biological Sciences, 2017, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837

► We previously described that PKA/GSKIP/GSK3Î² complex serves as a platform to anchor and phosphorylate Drp1 affecting mitochondria dynamics to provide neuroprotection. Recently, a known PKA/GSK3Î²… (more)

▼ We previously described that PKA/GSKIP/GSK3Î² complex serves as a platform to anchor and phosphorylate Drp1 affecting mitochondria dynamics to provide neuroprotection. Recently, a known PKA/GSK3Î² substrate, Tau, has been revealed its S409 phosphorylation is associating with the termination of neuron cells in Alzheimer disease. In this study, we attempt to extend that Tau phosphorylation is also mediated by PKA/GSKIP/GSK3Î² working complex. Our data showed that GSKIP-WT overexpression in SH-SY5Y cells increased phosphorylation of Tau S409 site (not S214; S262; S396; S404; T205 and T212 sites) over that of PKA- and GSK3Î² binding-defective mutants (V41/L45 and L130) under forskolin challenge, indicating that both PKA and GSK3Î² bindings may be associated to phosphorylate Tau at S409 site. Surprisingly, treatment with foskion in GSKIP-WT-overexpressing SH-SY5Y cells were significantly increase Tau phosphorylation at S409, suggesting that only PKA kinase activity, but not GSK3Î², is required in the GSKIP-mediated Tau phosphorylation. However, silencing of GSK3Î² resulted in a dramatic decrease in phosphorylation of Tau S409, revealing both GSKIP and GSK3Î² are crucial of PKA/GSKIP/GSK3Î²/Tau complex. Further, overexpressed kinase-dead GSK3Î² K85R (retains capacity to bind GSKIP) in SH-SY5Y cells, but not K85M (loss of capacity to bind GSKIP), has a higher Tau S409 phosphorylation, ensures that GSK3Î² acts solely as an anchor binding protein rather than its kinase activity in this signaling axis. Due to previous studies showed several different residues of Tau can be phosphorylated by PKA, we conducted In vitro kinase assay and provided two clear results: (1) As similar to early findings, PKA played a phosphorylation role on Ser409, Ser214 and Ser262 residues of Tau. (2) GSK3Î² provided a conformational shelter in PKA/GSKIP/GSK3Î²/Tau complex to harbor Tau Ser409 residue so that PKA is failed to phosphorylate Tau Ser409 residue. Furthermore, by using CRISPR/Cas9 system to produce APP WT/D678H and APP WT/WT ã APP D678H/D678H multifunctional stem cells (modified from an APP patient WT/D678H genotype), the results of analysis showed phosphorylation in Tau Ser262 and Ser214 residues and the Tau Ser409 intense phosphorylation in the brain of Alzheimerâs patients.. Coupling with previous findings of PKA suggested that the PKA/GSKIP/GSK3Î²/Tau complex may plays a key role on the development of Alzheimerâs disease. Taken together, our data provide compelling evidence to implicate that both GSKIP and GSK3Î² function as anchoring proteins to enhance cAMP/PKA/Tau axis signaling during Alzheimer pathogenesis. Advisors/Committee Members: Tsuey%22%29&pagesize-30">Cheng Jiin-Tsuey (chair), Hong Yi-Ren (committee member), Huang Chi-Ying (chair), Chiou Shean-jaw (chair).

Subjects/Keywords: PKA; Tau; Alzheimer disease; Human induced pluripotent stem (iPS) cells; AÎ² precursor protein (; GSK3Î²; GSKIP

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wang, Y. (2017). The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837

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

Chicago Manual of Style (16^th Edition):

Wang, Yin-Hsuan. “The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells.” 2017. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837.

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

MLA Handbook (7^th Edition):

Wang, Yin-Hsuan. “The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells.” 2017. Web. 07 Mar 2021.

Vancouver:

Wang Y. The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells. [Internet] [Thesis]. NSYSU; 2017. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837.

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

Council of Science Editors:

Wang Y. The cAMP/PKA-mediated Tau S409 phosphorylation through GSKIP/GSK3 axis in SH-SY5Y and iPS cells. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0404117-114837

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

NSYSU

3. 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)

Subjects/Keywords: Wnt pathway; Î²-catenin; Hepatocellular carcinoma; cellular signaling; LECT2

Record Details Similar Records Cite « Share

❌

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

APA (6^th 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 (16^th Edition):

Wu, Ping-Hsuan. “The role of LECT2 in liver carcinogenesis.” 2011. Thesis, NSYSU. Accessed March 07, 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 (7^th Edition):

Wu, Ping-Hsuan. “The role of LECT2 in liver carcinogenesis.” 2011. Web. 07 Mar 2021.

Vancouver:

Wu P. The role of LECT2 in liver carcinogenesis. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Mar 07]. 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

4. Chan, Yu-Lin. Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-1Î².

Degree: Master, Biological Sciences, 2012, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1113112-160654

► Grouper (Epinephelus coioides) is one of the important farmed fish in the southern Taiwan. However, grouper aquaculture in Taiwan has a serious problem of infection,… (more)

Subjects/Keywords: antiserum; lipopolysarcharide; fusion protein; IL -1Î²; Epinephelus coioides

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chan, Y. (2012). Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-1Î². (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1113112-160654

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

Chicago Manual of Style (16^th Edition):

Chan, Yu-Lin. “Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-1Î².” 2012. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1113112-160654.

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

MLA Handbook (7^th Edition):

Chan, Yu-Lin. “Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-1Î².” 2012. Web. 07 Mar 2021.

Vancouver:

Chan Y. Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-1Î². [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1113112-160654.

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

Council of Science Editors:

Chan Y. Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-Production and characterization of polyclonal antibody against Epinephelus coioides interleukin-1Î². [Thesis]. NSYSU; 2012. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1113112-160654

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 Î²-amyloid deposition frequently occuring altogether after chronic lead exposure. Recent studies have shown that the Î²-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 Î¼M for 1, 2, 3 and 4 days. Doses of lead acetate with of lead acetate were 5 Î¼M 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 AÎ²1-40 and AÎ²1-42 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 Î²-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), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (committee member), Tai,Ming-Hong (chair), Chen, Shun-Sheng (committee member).

Subjects/Keywords: Alzheimerâs Disease; amyloid precursor protein; autophagy; amyloidogensis disorders; apoptosis; Î²-amyloid protein; lead exposure

Record Details Similar Records Cite « Share

❌

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

APA (6^th 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 (16^th Edition):

Chen, Chueh-Tan. “The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure.” 2012. Thesis, NSYSU. Accessed March 07, 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 (7^th Edition):

Chen, Chueh-Tan. “The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure.” 2012. Web. 07 Mar 2021.

Vancouver:

Chen C. The Possible Role of Neuron Autophagy on Amyloidogenesis Disorderswith Lead Exposure. [Internet] [Thesis]. NSYSU; 2012. [cited 2021 Mar 07]. 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. Ming Yen, Liang. The Association of XRCC1 Polymorphisms with Development and Prognosis of Oral and Pharyngeal Squamous Cell Carcinomas.

Degree: Master, Biological Sciences, 2011, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825111-020128

► X-ray repair cross complementing Group 1 (XRCC1) protein plays an important role in base excision repair. Single nucleotide polymorphisms (SNPs) in XRCC1 gene may affect… (more)

▼ X-ray repair cross complementing Group 1 (XRCC1) protein plays an important role in base excision repair. Single nucleotide polymorphisms (SNPs) in XRCC1 gene may affect DNA repairing ability, genetic susceptibility, and prognosis to oral and pharyngeal squamous cell cancer (OPSCC). This study was carried out to evaluate the association of three XRCC1 SNPs with the risk and prognosis of OPSCC. A total of 509 OPSCC cases and 678 cancer-free controls were recruited to detect the genotypes of XRCC1 by PCR-RFLP. Then, 447 case patients with surgical treatment and safety margins were included in the survival analysis. No association was observed for XRCC1 194 and the risk of OPSCC. As compared with the wild Arg/Arg genotype, the combined genotypes of 280 Arg/His and His/His were with decreased risk (AOR=0.73, 95% CI, 0.52-1.03, p = 0.069) of OPSCC and with a significantly decreased risk (AOR=0.67, 95% CI, 0.47-0.97, p = 0.035) of oral cavity. As compared with the Arg/Arg genotype of XRCC1 399, the Gln/Gln genotype was with the increased risk of OPSCC (AOR=2.06, 95%CI: 1.21-3.51, p = 0.008) and oral cavity cancer (AOR=1.89, 95%CI: 1.08-3.33, p = 0.026). We defined the âputative high risk haplotypesâ as âArg-Arg-Gln and Trp-Arg-Glnâ. The AOR were 1.29 (95% CI, 1.04-1.60, p = 0.020) for the âputative high risk haplotypesâ as compared with other haplotypes for OPSCC. Then, two putative high risk haplotypes were combined into âputative high risk diplotypesâ. The AOR for the âhigh risk diplotypesâ were 1.98 (95% CI, 1.18-3.33, p = 0.010) as compared with other diplotypes for OPSCC. No association between XRCC1 polymorphisms and clinicopathological outcomes, except XRCC1 280. Those carriers of XRCC1 280His allele (combined Arg/His and His/His genotypes) were associated with late onset (≥50 yrs) of oral cavity cancers. No association between genetic variants in XRCC1 and disease-specific survival except XRCC1 399. Patients with 399 Arg/Gln and Gln/Gln genotypes showed a significant better survival as compared to Arg/Arg genotype carriers (AHR 0.41 95% CI: 0.18-0.93), especially for those patients younger than 50 years (p = 0.012), in pathological stage III or IV (p = 0.044), and without postoperative radiotherapy (p = 0.012). In summary, XRCC1 280 Arg/His and His/His genotypes were associated with decreased risk of oral cavity cancer. 399 Gln/Gln genotype was associated with increased risk of OPSCC and oral cavity cancer. The putative âhigh risk haplotypes and diplotypesâ were with increased risk of OPSCC. However, 399 Arg/Gln and Gln/Gln genotypes were prognostic factors, especially for those with young age, aggressive tumor stage, and without postoperative radiotherapy for oro and hypopharynx patients. These findings suggest that XRCC1 polymorphisms may play a role in the development and prognosis of OPSCC. Advisors/Committee Members: Shiue, Yow-Ling (chair), Cho, Chung-Lung (chair), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (committee member), Luo-Ping Ger (committee member).

Subjects/Keywords: prognosis; polymorphism; XRCC1; risk; OPSCC; oral cancer

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Ming Yen, L. (2011). The Association of XRCC1 Polymorphisms with Development and Prognosis of Oral and Pharyngeal Squamous Cell Carcinomas. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825111-020128

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

Chicago Manual of Style (16^th Edition):

Ming Yen, Liang. “The Association of XRCC1 Polymorphisms with Development and Prognosis of Oral and Pharyngeal Squamous Cell Carcinomas.” 2011. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825111-020128.

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

MLA Handbook (7^th Edition):

Ming Yen, Liang. “The Association of XRCC1 Polymorphisms with Development and Prognosis of Oral and Pharyngeal Squamous Cell Carcinomas.” 2011. Web. 07 Mar 2021.

Vancouver:

Ming Yen L. The Association of XRCC1 Polymorphisms with Development and Prognosis of Oral and Pharyngeal Squamous Cell Carcinomas. [Internet] [Thesis]. NSYSU; 2011. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825111-020128.

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

Council of Science Editors:

Ming Yen L. The Association of XRCC1 Polymorphisms with Development and Prognosis of Oral and Pharyngeal Squamous Cell Carcinomas. [Thesis]. NSYSU; 2011. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825111-020128

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), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (chair), Tai, ming-hong (committee member), Hsu, Ching-Mei (chair).

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

10 more images…

Record Details Similar Records Cite « Share

❌

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

APA (6^th 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 (16^th 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 March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0823111-140424.

MLA Handbook (7^th 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. 07 Mar 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 Mar 07]. 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. Tsui, Kuan-Hao. Effects of dehydroepiandrosterone supplementation on clinical outcomes and cumulus cells gene expression in women with poor ovarian response.

Degree: PhD, Biological Sciences, 2015, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0613115-115441

► The aim of the study was to investigate the effects of dehydroepiandrosterone (DHEA) supplementation on IVF (In vitro fertilization) outcomes and the gene expression of… (more)

▼ The aim of the study was to investigate the effects of dehydroepiandrosterone (DHEA) supplementation on IVF (In vitro fertilization) outcomes and the gene expression of cumulus cells (CCs) in patients with poor ovarian response (POR). This was a prospective self-controlled study, including ten patients with POR. All women received DHEA supplementation (30 mg, t.i.d.) for around 3 months before starting the a new IVF cycle. Biochemical, ultrasound parameters and treatment outcomes were determined before and after DHEA therapy. Moreover, CCs were isolated to examine the gene expression level of nine genes, including Hyaluronan synthase (HAS2), Versican (VCAN), Thrombospondin 1 (THBS1), Runt-related transcription factor 2 (RUNX2), Chromobox homolog 3 (CBX3), Tripartite motif-containing 28 (TRIM28), B-cell lymphoma 2 (BCL2), BCL2-associated X protein (BAX), Ankyrin repeat domain 57 (ANKRD57), Syndecan 4 (SDC4), Activated leukocyte cell adhesion molecule (ALCAM), Gremlin 1 (GREM1), Prostaglandin-endoperoxide synthase 1 (PTGS1), Prostaglandin-endoperoxide synthase 2 (PTGS2), Sprouty homolog 4 (SPRY4), Coagulation factor II receptor-like 1 (F2RL1), Ribosomal protein S6 kinase, polypeptide 2 (RPS6KA2), solute carrier family 38, member 2 (SLC38A2), YTH domain familyï¼member 2 (YTHDF2), Cytochrome oxidase 17 (COX17), E3 ubiquitin protein ligase (UBR3), Krueppel-like factor 4 (KLF4), prostaglandin E receptor 2 (PTGER2), exostoses 1 (EXT1) by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). It showed significant changes in day 3 follicle-stimulating hormone (FSH), estradiol, antral follicle count (AFC) and Anti-MÃ¼llerian Hormone (AMH) (p < 0.0001, < 0.0001, < 0.05 and < 0.001, respectively), as well as number of oocytes retrieved, fertilized oocytes, day 3 embryos, transferred embryos (p < 0.0001, < 0.0001, < 0.05 and < 0.001, respectively) after DHEA therapy. In addition, the gene expression levels of extracellular matrix (ECM), including HAS2, VCAN, THBS1, showed significant increase after DHEA treatment. Although the gene expression levels of BCL2 and BAX, which are apoptotic genes, showed decrease; however, BCL2/BAX ratio elevated significantly, suggested that DHEA may play a role in anti-apoptosis. The study demonstrated that DHEA shows benefit for artificial reproductive outcomes and upregulates the gene expression of CCs in POR patients. Advisors/Committee Members: Chen Chun-Lin (chair), Wen Zhi-Hong (chair), Tsuey%22%29&pagesize-30">Cheng Jiin-Tsuey (committee member), Chang Shiuh-Young (chair), Wang Peng-Hui (chair).

Subjects/Keywords: DHEA; cumulus cells; Dehydroepiandrosterone; diminished ovarian reserve

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Tsui, K. (2015). Effects of dehydroepiandrosterone supplementation on clinical outcomes and cumulus cells gene expression in women with poor ovarian response. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0613115-115441

Chicago Manual of Style (16^th Edition):

Tsui, Kuan-Hao. “Effects of dehydroepiandrosterone supplementation on clinical outcomes and cumulus cells gene expression in women with poor ovarian response.” 2015. Doctoral Dissertation, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0613115-115441.

MLA Handbook (7^th Edition):

Tsui, Kuan-Hao. “Effects of dehydroepiandrosterone supplementation on clinical outcomes and cumulus cells gene expression in women with poor ovarian response.” 2015. Web. 07 Mar 2021.

Vancouver:

Tsui K. Effects of dehydroepiandrosterone supplementation on clinical outcomes and cumulus cells gene expression in women with poor ovarian response. [Internet] [Doctoral dissertation]. NSYSU; 2015. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0613115-115441.

Council of Science Editors:

Tsui K. Effects of dehydroepiandrosterone supplementation on clinical outcomes and cumulus cells gene expression in women with poor ovarian response. [Doctoral Dissertation]. NSYSU; 2015. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0613115-115441

NSYSU

9. Chen, Heng-Chi. Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin.

Degree: Master, Biological Sciences, 2000, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039

► Antiangiogenic tomor therapies have attracted intense interest for their broad-spectrum action, low toxicity, and in the case of direct endothelial targeting, an absence of drug… (more)

▼ Antiangiogenic tomor therapies have attracted intense interest for their broad-spectrum action, low toxicity, and in the case of direct endothelial targeting, an absence of drug resistance. Among the growing list of antiangiogenic agents, endostatin has attracted most attention and been under the spotlight of numerous debates. Like other angiogenesis inhibitors, endostatin is also a proteolytic fragment (~20 kDa) from an extracellular protein, collagen XVIII. It potently inhibits endothelial cell proliferation and angiogenesis, but has no cytotoxic effects on cancer cells. Above all, therapy of experimental cancer with endostatin in rodents leads to tumor dormancy and does not induce resistance. However, the exact mechanism on how endostatin inhibited endothelial cells proliferation remains largely unknown. We have cloned mouse endostatin cDNA from mice liver by RT-PCR. After verification by DNA sequencing, endostatin cDNA was subcloned in to E.coli expression vector to express and generate large quantities of recombinant GST-fused endostatin (GST-endostatin). Unlike His-tagged endostatin, GST-endostatin is soluble and capable of inhibiting various endothelial cell lines including HUVEC, EA.hy926 and BAEC with IC50 ~ 20 nM. Flow cytometry analysis indicated GST-endostatin induced apoptosis in EA.hy926 cells. GST-endostatin also inhibited the cell migration of EA.hy926 cells toward chemoattractant bFGF with IC50 ~ 0.5 nM. Further more, GST-endostatin inhibited in vivo angiogenesis in chicken chorioallantoic membrane and suppressed tumor growth in mice bearing Lewis lung carcinoma cells. After functional characterization of GST-endostatin, we decided to use GST-endostatin and EA.hy926 cells as a model system to study the inhibitory mechanism of endostatin in endothelial cells. By using fura-2 fluorescence probe, GST-endostatin was shown to elevate the cytosolic calcium in dose-dependent manner from extracellular source. Chelation of extracellular Ca2+ by EGTA or inhibition of calcium channel by nifedipine abolished the cytotoxic effect endostatin, suggesting the calcium rise by endostatin play an important role in its inhibitory mechanism. Besides, endostatin also stimulated activity of a large- conductance calcium-activated potassium (Bkca) channel, further supporting endostatin initiated serial changes in ion channels activities in endothelial cells. Respiratory enzyme activities and endogenous ATP synthesis in endothelial cells were significantly inhibited by GST-endostatin treatment, indicating GST-endostatin depleted the energy source for endothelial cells. In summary, present study demonstrated GST-endostatin caused dramatic changes in electrophysiologic properties and decreased endogenous ATP synthesis in endothelial cells, which may participate in its inhibitory mechanism. Advisors/Committee Members: Shiuan, David (chair), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (committee member), Hong Yi-Ren (chair), Ming-Hong Tai (committee member).

Subjects/Keywords: angiogenesis; endostatin

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chen, H. (2000). Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039

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

Chicago Manual of Style (16^th Edition):

Chen, Heng-Chi. “Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin.” 2000. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039.

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

MLA Handbook (7^th Edition):

Chen, Heng-Chi. “Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin.” 2000. Web. 07 Mar 2021.

Vancouver:

Chen H. Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin. [Internet] [Thesis]. NSYSU; 2000. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039.

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. Studies on the Inhibitory Mechanism of Angiogenesis Inhibitor, Endostatin. [Thesis]. NSYSU; 2000. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0704100-014039

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

NSYSU

10. Sy, Wei-Dih. Analysis of human Dynamin IV (Dymple) gene promoter.

Degree: Master, Biological Sciences, 2003, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445

► We first identified the transcriptional regulatory element of the human dynamin IV gene (Hdyn IV; dymple). The Hdyn IV belongs to a large GTPase family.… (more)

▼ We first identified the transcriptional regulatory element of the human dynamin IV gene (Hdyn IV; dymple). The Hdyn IV belongs to a large GTPase family. This protein has a N-terminal highly conserved tripartite GTP-binding domain, coiled-coil (CC) region, but it lacks the pleckstrin homology (PH) domain and a modestly conserved C-terminal proline rich domain (PRD). Hdyn IV gene is enriched in subcellular membrane fractions of cytoplasmic vesicles and endoplasmic reticulum, and the function of Hdyn IV gene is considered to be associated with the functions of mitochondria. The Hdyn IV is expressed as four alternative splicing variants in all eukaryotic organisms. Our question concerning why expressions of four alternative splicing variants in brain tumor tissues? To elucidate the regulatory mechanism and the transcription factors involved, we firstly determined the transcriptional start site by 5â RACE. We next cloned the 5â-flanking region of the Hdyn IV gene and determined the nucleotide sequence of 999 bases upstream from the transcription start site. The promoter has several potential binding sites for AP2, Sp1 binding protein, but it lacks TATA and CAAT boxes. Transfection studies using a series of Hdyn IV promoter luciferase constructs in HeLa cell demonstrate that the 5âflanking region has a promoter activity. Functional promoter element of the Hdyn IV gene was located within the â140~ +29 region. Deletion analyses demonstrated that the minimal promoter activity for the transcriptional element of Hdyn IV was detected in the sequence between nucleotides â110 and â100. Electorphoretic mobility shift assay demonstrated that a putative transcriptional factor bound to the â119 to â90 region. Site-directed mutagenesis analysis of this region revealed that nucleotides at positions â108 to â100 were essential for transactivation mediated by this element. To summary, the data indicated that the ââCTCCCAGCAââ (-108~ -100) sequence is capable of regulating Hdyn IV gene expression. However, the protein involved in the binding of this novel sequence requires further study. Advisors/Committee Members: Hsu, Ching-Mei (chair), Hong, Yi-Ren (committee member), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (chair), Cho, Chung-Lung (committee member).

Subjects/Keywords: transcription factor; promoter; DynIV

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Sy, W. (2003). Analysis of human Dynamin IV (Dymple) gene promoter. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445

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

Chicago Manual of Style (16^th Edition):

Sy, Wei-Dih. “Analysis of human Dynamin IV (Dymple) gene promoter.” 2003. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445.

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

MLA Handbook (7^th Edition):

Sy, Wei-Dih. “Analysis of human Dynamin IV (Dymple) gene promoter.” 2003. Web. 07 Mar 2021.

Vancouver:

Sy W. Analysis of human Dynamin IV (Dymple) gene promoter. [Internet] [Thesis]. NSYSU; 2003. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445.

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

Council of Science Editors:

Sy W. Analysis of human Dynamin IV (Dymple) gene promoter. [Thesis]. NSYSU; 2003. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0904103-145445

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

NSYSU

11. Wu, Mei-jen. The mechanisms of isoobtusilactone A-induced apoptosis in human hepatoblastoma cell line (Hep G2).

Degree: Master, Biological Sciences, 2007, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0728107-113601

► Chemoprevention using naturally occurring substances has now been considered a promising strategy for the prevention of cancer. In this study, the effects of isoobtusilactone A,… (more)

▼ Chemoprevention using naturally occurring substances has now been considered a promising strategy for the prevention of cancer. In this study, the effects of isoobtusilactone A, a novel constituent isolated from the leaves of Cinnamomum kotoense, on the proliferation of human hepatoma Hep G2 cells and the underlying mechanisms in isoobtusilactone A-induced apoptosis are thoroughly evaluated. Under the experimental conditions adapted by this study, isoobtusilactone A was found to exhibit a concentration-dependent growth impediment (IC50 = 37.5 Î¼M). The demise of the cells induced by isoobtusilactone A was apoptotic in nature, showing progressive sub-G1 fraction and DNA fragmentation when the concentration of the substrate was increased. Subcellular fractionation analysis further revealed that Bax translocation to mitochondria resulted in a rapid release of cytochrome c, followed by the activation of caspase 3 and PARP cleavage, and finally cell death. Isoobtusilactone A-treated cells also displayed transient increase of ROS during the earlier stage of the experiment, followed by the disruption of mitochondrial transmembrane potential ( m). The presence of a ROS scavenger (N-acetyl-L-cysteine,NAC) and an inhibitor of NADPH oxidase (diphenyleneiodonium chloride,DPI) blocked ROS production and the subsequent apoptotic cell death. Taken together, our data suggest that ROS generated through the activation of NADPH oxidase plays an essential role in apoptosis induced by isoobtusilactone A. To clarify whether caspases were the sole mediators for eliciting the observed apoptotic process, the effects of a broad caspases inhibitor, Z-VAD.fmk, was studied. Interestingly, Z-VAD.fmk was found to completely inhibit the isoobtusilactone A-induced oligonucleosomal DNA fragmentation, yet it could only prevent limited amount of cells from becoming apoptosis-prone. These data implied that other mechanism(s) might also be important factors and led us to study the possible involvement of apoptosis-inducing factor (AIF), a mediator arbitrating caspase-independent apoptosis, in isoobtusilactone A-induced apoptotic process. Our data indicated that isoobtusilactone A could elicit the nuclear translocation of AIF observed along with the occurrence of large-scale DNA fragmentation. Reduction of AIF expression by AIF-siRNA transfection suppressed large-scale DNA fragmentation. Interestingly, inhibition of AIF expression by AIF-siRNA did not prevent isoobtusilactone A-induced oligonucleosomal DNA fragmentation. When the cells were simultaneously treated with AIF-siRNA and Z-VAD.fmk, both large-scale DNA and oligonucleosomal DNA fragmentations were almost completely prevented. In conclusion, our data suggest that isoobtusilactone A induced apoptotic cell death was caused by the increase of ROS, followed by the disruption of mitochondrial transmembrane potential ( m), further mediated by both caspase-dependent and caspase-independent pathways. Advisors/Committee Members: Liu, Tsan-Zon (chair), Chern, Chi-Liang (committee member), Liu, Ray-H. (chair), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (committee member).

Subjects/Keywords: Isoobtusilactone A

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wu, M. (2007). The mechanisms of isoobtusilactone A-induced apoptosis in human hepatoblastoma cell line (Hep G2). (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0728107-113601

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

Chicago Manual of Style (16^th Edition):

Wu, Mei-jen. “The mechanisms of isoobtusilactone A-induced apoptosis in human hepatoblastoma cell line (Hep G2).” 2007. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0728107-113601.

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

MLA Handbook (7^th Edition):

Wu, Mei-jen. “The mechanisms of isoobtusilactone A-induced apoptosis in human hepatoblastoma cell line (Hep G2).” 2007. Web. 07 Mar 2021.

Vancouver:

Wu M. The mechanisms of isoobtusilactone A-induced apoptosis in human hepatoblastoma cell line (Hep G2). [Internet] [Thesis]. NSYSU; 2007. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0728107-113601.

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

Council of Science Editors:

Wu M. The mechanisms of isoobtusilactone A-induced apoptosis in human hepatoblastoma cell line (Hep G2). [Thesis]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0728107-113601

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

NSYSU

12. Chia-Yi, Hou. Ras mutations in thyroid neoplasia.

Degree: Master, Biological Sciences, 2002, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0926102-011452

► Abstrate: Ras proto-oncogenes are members of the superfamily of GTP-binding proteins. Many tyrosine kinase receptors, including those for epidermal growth factor, insulin, and nerve growth… (more)

▼ Abstrate: Ras proto-oncogenes are members of the superfamily of GTP-binding proteins. Many tyrosine kinase receptors, including those for epidermal growth factor, insulin, and nerve growth factor, signal through RAS proteins. The product of members of this oncogene family (H-, K-, N-ras) is a 21 kD protein with nucleotide binding activity, involved in the transduction of information from the cell surface to the nucleus. The three RAS proteins exit in two states: a resting state in which they are bound to GDP and an active state in which they bind GTP. The most common form of mutational activation of Ras oncogenes in human tumors is through single base substations affecting either the GTP-binding of main (codons 12 and 13) or the GTPase domain (codon 61) of the protein. Thus, mutant RAS proteins result in constitutive activation of the downstream signaling cascade because their affinity for GTP is increased or their GTPase activity is decreased, so that the protein cannot return to the resting state. To investigate we have screened 89 thyroid tumor specimens, which include 8 follicular carcinomas (FC), 42 papillary carcinoma (PTC), 2 anaplastic carcinoma (AC),5 Hurthle cell adenoma (HA), 12 follicular adenoma (FA) and 20 nodular goiter (NG), for mutation in three Ras genes using PCR and automatic sequencing. Four tumors contained Ras gene mutation. Of these, three were identified among FC (37.5%), which mutation were in the codon 61 of each Ras genes. One mutation were at codon 61 of N-ras in FA specimens (8.3%). In addition, 33.7% (30/89) of specimens contain H-ras codon 27 polymorphism. In conclusion, our data indicated that the prevalence rates of Ras gene mutation were 5.8% and 2.7% in thyroid carcinoma and thyroid benign adenoma, respectively. Other environmental or genetic factors might also involved in the thyroid tumorigenesis and worth further investigation. The data were further confirmed using the combination of the PCR and denaturing gradient gel electrophoresis (DGGE). Four more cases of possible Ras mutation were detected which did not revealed by automatic sequencing , indicating that DGGE is a more sensitive method in detecting single nucleotide mutation. DGGE analysis should increase the detection rate of Ras gene mutation in our analysis. Advisors/Committee Members: Tsuey%22%29&pagesize-30">Cheng Jiin-Tsuey (committee member), Liu Rue-Tsuan (chair), Liu Jong-Kang (chair).

Subjects/Keywords: thyroid tumor; PCR; sequencing; DGGE; Ras gene

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chia-Yi, H. (2002). Ras mutations in thyroid neoplasia. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0926102-011452

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

Chicago Manual of Style (16^th Edition):

Chia-Yi, Hou. “Ras mutations in thyroid neoplasia.” 2002. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0926102-011452.

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

MLA Handbook (7^th Edition):

Chia-Yi, Hou. “Ras mutations in thyroid neoplasia.” 2002. Web. 07 Mar 2021.

Vancouver:

Chia-Yi H. Ras mutations in thyroid neoplasia. [Internet] [Thesis]. NSYSU; 2002. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0926102-011452.

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

Council of Science Editors:

Chia-Yi H. Ras mutations in thyroid neoplasia. [Thesis]. NSYSU; 2002. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0926102-011452

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

NSYSU

13. Wu, Jing-yi. Chibby Acts as a Tumor Suppressor and Beta-catenin Antagonist present in the Nucleus and Cytoplasm of HeLa cells.

Degree: Master, Biological Sciences, 2006, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710106-130223

► ABSTRACT Chibby (or PIGEA-14) is a novel antagonist of the Beta-catenin pathway in nucleus. However, the tumor-suppressing function of Chibby and the importance of nuclear… (more)

Subjects/Keywords: Chibby; AXIN; HeLa cell; Beta-catenin; APC; Tumor suppressor

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Wu, J. (2006). Chibby Acts as a Tumor Suppressor and Beta-catenin Antagonist present in the Nucleus and Cytoplasm of HeLa cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710106-130223

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

Chicago Manual of Style (16^th Edition):

Wu, Jing-yi. “Chibby Acts as a Tumor Suppressor and Beta-catenin Antagonist present in the Nucleus and Cytoplasm of HeLa cells.” 2006. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710106-130223.

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

MLA Handbook (7^th Edition):

Wu, Jing-yi. “Chibby Acts as a Tumor Suppressor and Beta-catenin Antagonist present in the Nucleus and Cytoplasm of HeLa cells.” 2006. Web. 07 Mar 2021.

Vancouver:

Wu J. Chibby Acts as a Tumor Suppressor and Beta-catenin Antagonist present in the Nucleus and Cytoplasm of HeLa cells. [Internet] [Thesis]. NSYSU; 2006. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710106-130223.

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

Council of Science Editors:

Wu J. Chibby Acts as a Tumor Suppressor and Beta-catenin Antagonist present in the Nucleus and Cytoplasm of HeLa cells. [Thesis]. NSYSU; 2006. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0710106-130223

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

NSYSU

14. Lin, James. The Differential Expression of Bcl10 in the Tumor Cell Lines.

Degree: Master, Biological Sciences, 2004, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835

► Bcl10 is one of the apoptosis regulatory protein. It is located at 1p22,one site harbor tumor suppressor tumor gene. We screen Bcl10 expression in different… (more)

Subjects/Keywords: tumor suppressor tumor gene

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Lin, J. (2004). The Differential Expression of Bcl10 in the Tumor Cell Lines. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835

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

Chicago Manual of Style (16^th Edition):

Lin, James. “The Differential Expression of Bcl10 in the Tumor Cell Lines.” 2004. Thesis, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835.

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

MLA Handbook (7^th Edition):

Lin, James. “The Differential Expression of Bcl10 in the Tumor Cell Lines.” 2004. Web. 07 Mar 2021.

Vancouver:

Lin J. The Differential Expression of Bcl10 in the Tumor Cell Lines. [Internet] [Thesis]. NSYSU; 2004. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835.

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

Council of Science Editors:

Lin J. The Differential Expression of Bcl10 in the Tumor Cell Lines. [Thesis]. NSYSU; 2004. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0816104-155835

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

NSYSU

15. 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), Tai Ming-Hong (committee member), Tsuey%22%29&pagesize-30">Cheng Jiin-Tsuey (chair), Chuang Jiin-Haur (committee member).

Subjects/Keywords: overexpression; tumorigenicity; hepatoma cells; Dlk protein

Record Details Similar Records Cite « Share

❌

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

APA (6^th 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 (16^th Edition):

Wu, Chia-Ling. “The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.” 2004. Thesis, NSYSU. Accessed March 07, 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 (7^th Edition):

Wu, Chia-Ling. “The effect of Dlk overexpression on the tumorigenicity of hepatoma cells.” 2004. Web. 07 Mar 2021.

Vancouver:

Wu C. The effect of Dlk overexpression on the tumorigenicity of hepatoma cells. [Internet] [Thesis]. NSYSU; 2004. [cited 2021 Mar 07]. 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

NSYSU

16. Chen, Rong-fu. Immunopathogenesis of dengue-2 infection in a dengue-2 outbreak.

Degree: PhD, Biological Sciences, 2007, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0908107-120338

► Incidence of dengue fever (DF) has been estimated a 30 fold increase in the past 50 years. Clinical manifestations of DF range from a simple… (more)

▼ Incidence of dengue fever (DF) has been estimated a 30 fold increase in the past 50 years. Clinical manifestations of DF range from a simple febrile illness with physical soreness to life-threatening dengue hemorrhagic fever (DHF). The need for a better classification of the severity in DEN infections has been proposed to clarify the immunopathogenesis for the prevention and management of serious DEN infections. We attempted to investigate whether different mechanisms involved in the varied manifestations of bleeding tendency and vascular leakage in DF. In a hospital-based study, we first compared clinical features as well as laboratory data including virus load, T helper (Th1/Th2) cytokines, and vascular leakage-related mediators between patients with DHF and DF. Moreover, we defined another class of patients associated with bleeding tendency but not fulfilled with DHF criteria, called DF w/B, for a further comparison. The virus load in blood was not significantly different among DF, DHF and DF w/B. DF patients had a higher Th1 cytokine, IFNr, expression (70.0 Â± 10.7 vs. 33.1 Â± 8.0 vs. 33.0 Â± 7.1 pg/ml; DF vs. DF w/B, p = 0.009; DF vs. DHF, p = 0.002), and both DHF and DF w/B patients had a significantly higher IL-10 levels (14.3 Â± 4.1 vs. 26.2 Â± 3.3 vs. 26.0 Â± 3.5 pg/ml; DF vs. DF w/B, p = 0.023; DF vs. DHF, p = 0.016) than DF patients. Both DHF and DF w/B patients also had a higher rate of secondary dengue infection (DF w/B vs. DHF vs. DF: 50.0%, 74.4% and 14.3%ï¼ p < 0.001). By contrast, DHF but not DF w/B patients had significantly higher vascular leakage-related mediators: sVCAM-1, PGE2 and TNFÎ± levels than DF patients. Patients with DF w/B had a higher platelet counts (DF w/B vs. DHF: 66.0 Â± 8.3 vs. 20.7 Â± 2.1 x109/L, p < 0.001) but lower ALT levels than those with DHF (DF w/B vs. DHF: 56.3 Â± 7.7 and 144.7 Â± 20.5 IU/L). This study provides new insight to different immune mechanisms involved in patients with DF, DF w/B, and DHF. DF involves augmented Th1 reaction, and DF w/B involves altered Th2 reaction, but DHF involves both altered Th2 reaction and augmented vascular insult. Clarification of the immune mechanisms among DF, DFw/B and DHF will facilitate certain specific treatment and prevention of DF patients from varied bleeding tendency and vascular leakage manifestations. Advisors/Committee Members: Liu, Jong-Kang (chair), Yang, Kuender D. (committee member), He, Shiping (chair), none (chair), Hung, WC (chair), Tsuey%22%29&pagesize-30">Cheng, Jiin-Tsuey (committee member).

Subjects/Keywords: dengue hemorrhagic fever; secondary infection; dengue fever; immunopathogenesis; cytokine

Record Details Similar Records Cite « Share

❌

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

APA (6^th Edition):

Chen, R. (2007). Immunopathogenesis of dengue-2 infection in a dengue-2 outbreak. (Doctoral Dissertation). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0908107-120338

Chicago Manual of Style (16^th Edition):

Chen, Rong-fu. “Immunopathogenesis of dengue-2 infection in a dengue-2 outbreak.” 2007. Doctoral Dissertation, NSYSU. Accessed March 07, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0908107-120338.

MLA Handbook (7^th Edition):

Chen, Rong-fu. “Immunopathogenesis of dengue-2 infection in a dengue-2 outbreak.” 2007. Web. 07 Mar 2021.

Vancouver:

Chen R. Immunopathogenesis of dengue-2 infection in a dengue-2 outbreak. [Internet] [Doctoral dissertation]. NSYSU; 2007. [cited 2021 Mar 07]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0908107-120338.

Council of Science Editors:

Chen R. Immunopathogenesis of dengue-2 infection in a dengue-2 outbreak. [Doctoral Dissertation]. NSYSU; 2007. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0908107-120338

		in
And / Or
		in
And / Or
		in
And / Or
		in

Open Access Theses and Dissertations